Evolution is a scam

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Sorrentino's picture
Evolution is a scam

The theory of evolution should be expunged from curriculum of biology.

In order to fully explain the origin of different plants and animals that exist on the earth, all various theories of evolution ( neo-darwinian model, punctuated equilibrium model and neutral model of molecular evolution) completely focus on how the genetic information contained in the DNA are being "changed" or "rewired" by mutations (as the theories assumed).

Not only that these evolutionary theories completely neglect how the first complete set of DNA information ( contained in the first living cell ) came to exist in the first place, but they also completely neglect the ultimate origin of the underlying design ( like meiotic cell division, fertilization, mitotic cell division, cellular differentiation and morphogenesis ) that even make the transformation of these DNA information into physical plants and animals to be possible.

Hence, the similitude of the evolutionary scientists are like researchers who completely focus on how the instructions contained in the cooking manual are being changed in order to fully explain the origin of the varieties of food found in a particular restaurant and completely neglect how those cooking instructions are being actually transformed into different plates of food served before the customers.

Yet it is agreed by all that the underlying design ( a well- furnished kitchen with cooking utensils, cooking appliances, cooking ingredients and cooking experts that would read, interpret and implement the cooking instructions ) that make the transformation of instructions contained in the cooking manual into different plates of food to be possible is far far more important than the cooking instructions itself.

Similarly, the underlying design ( like meiotic cell division, fertilization, mitotic cell division, cellular differentiation and morphogenesis) that make the transformation of the DNA information into physical plants and animals to be possible is far far more important than the DNA information itself

(1)If this is true, then why do all the theories of evolution completely focus on how the genetic information contained in the DNA are being "changed" or "rewired" by mutations (as the theories assumed) in order to fully explain the origin of different plants and animals and completely neglect the ultimate origin of the underlying design (like meiotic cell division, fertilization, mitotic cell division, cellular differentiation and morphogenesis) that make the transformation of these DNA information into physical plants and animals to be possible ?

Even if we assume that the first living cell managed to evolve from non living materials and again managed to replicate itself ( abiogenesis—a problem that all the world scientists are yet to be solved), then:

(2) What later caused some of these self-replicating cells to abandon their diploid way of life and suddenly change to become haploid cells (meiotic cell division)—an event that make sexual reproduction to be possible— ?

( 3) What later caused two of these haploid cells to start fusing with one another during sexual reproduction in order to restore their original diploid state ( fertilization) ?

(4) What later caused this fused cell (called zygote) to multiply and form a compact ball of similar cells (mitotic cell division) ?

(5) What later caused this compact ball of similar cells to "differentiate" and "specalize" to form different types of cell (like bone cells, muscle cells, blood cells, nerve cells, skin cells, cartilage cells, epithelial cells, endothelia cells, liver cells, kidney cells, brain cells, retinal cells etc) using a complex cascade of genetic program known as developmental gene regulatory network (dGRN) ( cellular differentiation) ?

(6) What if the similar ball of cells just continue to multiply (like what we observed with cancer cells ) and never stop to start differentiation process ?

(7) Besides, how did last ball of cell to multiply get to "know" that it is time to stop multiplication and start the differentiation process ?

(8 What later caused these group of differentiated and specialized cells to start "arranging" themselves in a particular way in order to form various tissues and distinct organs of different size, shape and function at different location ( morphogenesis) ?

(9) What if all the differentiated cells just come together to form a big mass of intermingled tissue (like a bulk of shapeless meat) without forming any distinct organ ?

(10) So how does these differentiated cells "know" which direction to take, which pattern of arrangement to follow and to what extent they will multiply in order to construct a distinct organ of a particular shape and size in a specific location ?

(11) If all this knowledge regarding the shape, size and location of a particular organ in a body plan are already encoded in the genetic information, then what or better yet who encoded this knowledge ? And how does the cells even manage to decode this knowledge and act accordingly if there is no any "intelligent planning" that went ahead the whole show ?

If evolutionary scientists have no convincing answers to all these questions and even have no convincing explanation concerning the origin of the first living cell, then why does theory of evolution is still being portrayed in the academic circle as a scientific fact that fully explain how different plants and animals on earth came to exist without the need of being created by anyone ?

Is it not the high time for the theory of evolution to be completely expunged from the curriculum of biology both at the high school level and in colleges?

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Sorrentino's picture
Of course, some people may

Of course, some people may want to argue: if the theory of evolution is not true and we are truly created by someone intelligent, then why do we "sometimes" observe some birth defects and congenital anomalies in the newborn babies ?

The existence of birth defects and congenital anomalies that seldom observe in newborn babies is meant to prove
that hundreds of complex events involved in the transformation of a tiny ball of cell (called zygote) into a newborn baby is neither (i) the work of natural laws nor (ii) the work of random chance but (iii) the work of intelligent design.

For if those hundreds of complex embryonic events is the work of natural laws, then no birth defects would be observed because there is no way for the physical or chemical laws of nature to change to cause such anomalies in the newborn babies . For if the physical or chemical laws of nature are changeable, then a stable universe cannot exist.

Again, if those hundreds of complex events is the work of random chance, then the number of such anomalies in the newborn babies would be far far greater than the number of normal births. In fact, all newborn babies must posses one birth defect or the other . But this is not the case[b].

But could those hundreds of complex embryonic events be the [b]work of natural laws and the work of random chance combined together ?

If an event operate by obeying a work of natural laws, then such an event can only happen in one way. Hence, such an event cannot be based on a work of chance which required an event to happen in more than one way. Therefore, work of natural laws and work of chance directly contradict each other. Hence, both of them cannot just operate together in the same event. One must leave for the other to operate Hence, to assert that an embryonic event is due to work of natural laws and work of random chance combined together is nothing but contradiction in terms.

However, if we go extreme to assume that some of the embryonic events are purely base on the work of natural laws while other events are purely base on the work of random chance, then the number of birth defects would be roughly equal to the number of normal birth. Again, this is not the case: the number of normal births is far far greater than the number of birth defects.

Therefore, after the elimination of the work of natural laws and the work of random chance,[/b]then the only option left to account for those hundreds of complex embryonic events is the [b]work of intelligent design.

This is exactly how the birth defects and congenital anomalies that we sometimes observe in the newborn babies prove that complex events involved in the transformation of a zygote into a beautiful new born baby is the work of intelligent design.

But if you're not satisfy with this answer and you still insist that evolution is true and creation is false, then invite any evolutionary scientists to answer all the questions cited above (especially question 10 and 11).

Nyarlathotep's picture
Sorrentino - If an event

Sorrentino - If an event operate by obeying a work of natural laws, then such an event can only happen in one way.

That is the most ridiculous statement I've read this week; but hey it's only Monday.

xenoview's picture

Do you believe other animals are intelligently designed? What objective evidence do you have that there is an intelligent designer?

David Killens's picture
@ Sorrentino

@ Sorrentino

"Again, if those hundreds of complex events is the work of random chance, then the number of such anomalies in the newborn babies would be far far greater than the number of normal births. In fact, all newborn babies must posses one birth defect or the other . But this is not the case[b]."

What is the "[b]" for? Did you copy and paste from another source?

Your thinking classifies all changes as birth DEFECTS. On that I disagree because if you have siblings, each one is distinct from another. Every newborn has changes, the bisexual reproduction process is not one of cloning. And not all changes are lethal, gross, or malignant. Some changes are benign, some are even advantageous.

Randomhero1982's picture
Well one can argue, what is

Well one can argue, what is the better model.. a bayesian probability approach to evolutionary theory, in which we know 99% and that's currently good enough (but continue to search) or a god of the caps arguement which requires the suspension of all known laws I.e. physics.

If you believe creation is true, please provide empirical evidence to support your assertion.

Tin-Man's picture
@Sorrentino Re: OP

@Sorrentino Re: OP

Oh fuck-a-doddle-do... *face palm*... *groan*... Here we go again. The ol' Evolution Denial routine... *heavy sigh*... Okay, fine. Whatever. Well, safe to say there will be others along shortly to properly school you. Personally, I would love to do so myself, but I am no expert in that field of study. More to the point, though, it is not even remotely necessary for me to be highly knowledgeable in that area, because my being an atheist is remarkably independent of anything having to do with evolution or Abiogenisis. I am now an atheist strictly because of what is in the bible and how I was raised in a Christian home/community. All the current findings in the realm of evolution, Abiogenisis, bible development, and astrophysics serve only to reinforce my position. However, even if you were somehow able to completely debunk evolution with your very next post, I would STILL BE an atheist. Because your proving evolution to be wrong DOES NOT prove, or even indicate, the existence of your god.

So, what else ya got, Sparky?

(Side note: By the way, which of you godless heathens out there know how to do the text search thing? I could be totally wrong, but much of our new friend's material has a very "cut-n-paste" feel to it without giving proper credit. Just a hunch... *shrugging shoulders*...)

Simon Moon's picture


OK, so lets say you overturn all of what is known of evolutionary biology, and prove evolution wrong. That does not get you one step closer to demonstrating a god exists. You do understand that atheism existed long before Darwin came up with his theory, right?

Your 'god did it' hypothesis has to be supported with demonstrable, repeatable and falsifiable evidence (and valid and sound logic), on its own merits, whether evolution is correct of not.

So, your entire opening posts are pretty much non-sequiturs.

LostLocke's picture
Kinda looks like a giant copy

Kinda looks like a giant copy and paste OP. Or maybe that's just me, but it sure sounds extremely familiar...

Tin-Man's picture
@LostLocke Re: Cut-n-paste

@LostLocke Re: Cut-n-paste

Oh, good. Wasn't just my imagination.

CyberLN's picture
Sorrentino, you wrote, “But

Sorrentino, you wrote, “But if you're not satisfy with this answer and you still insist that evolution is true and creation is false, then invite any evolutionary scientists to answer all the questions cited above (especially question 10 and 11).”

NO! Do it yourself!

Grinseed's picture
You arent condeming

You arent condeming evolutionary theory because you think its wrong. You exhibit too little understanding of research of recent decades to propose any meaningful critiques.
You are simply and ineffectively defending your unverifiable belief in creation mythology.
What viable objective evidence do you have for a supernatural deity?

Calilasseia's picture
Oh look, another Gish Gallop

Oh look, another Gish Gallop from a pedlar of creationist masturbation fantasies.

Let's deal with the requisite assertions in turn, shall we?

In order to fully explain the origin of different plants and animals that exist on the earth, all various theories of evolution ( neo-darwinian model, punctuated equilibrium model and neutral model of molecular evolution) completely focus on how the genetic information contained in the DNA are being "changed" or "rewired" by mutations (as the theories assumed).

Mutations aren't "assumed", they're documented. Out of the 1½ million peer reviewed scientific papers in circulation from the field of evolutionary biology, tens of thousands of them document mutations that were observed to appear in various lineages, and many of those papers provide a genetic audit trail for those mutations. Among the favourite examples of mine are:

Nonhepatic Origin of Notothenioid Antifreeze Reveals Pancreatic Synthesis As Common Mechanism in Polar Fish Freezing Avoidance by Chi-Hing C Cheng, Paul A. Cziko and Clive W. Evans, Proceedings of the National Academy of Sciences of the USA, 103: 10491-10496 (2006) [Full paper downloadable from here]

Evolution of Antifreeze Glycoprotein Gene from a Trypsinogen Gene in Antarctic Notothenioid Fish by Liangbiao Chen, Arthur L. DeVries, and Chi-Hing C. Cheng, Proceedings of the National Academy of Sciences of the USA, 94*8): 3811-3816 (DOI: 10.1073/pnas.94.8.3811) [Full paper downloadable from here

Let's take a look at the latter paper shall we?

Freezing avoidance conferred by different types of antifreeze proteins in various polar and subpolar fishes represents a remarkable example of cold adaptation, but how these unique proteins arose is unknown. We have found that the antifreeze glycoproteins (AFGPs) of the predominant Antarctic fish taxon, the notothenioids, evolved from a pancreatic trypsinogen. We have determined the likely evolutionary process by which this occurred through characterization and analyses of notothenioid AFGP and trypsinogen genes. The primordial AFGP gene apparently arose through recruitment of the 5′ and 3′ ends of an ancestral trypsinogen gene, which provided the secretory signal and the 3′ untranslated region, respectively, plus de novo amplification of a 9-nt Thr-Ala-Ala coding element from the trypsinogen progenitor to create a new protein coding region for the repetitive tripeptide backbone of the antifreeze protein. The small sequence divergence (4–7%) between notothenioid AFGP and trypsinogen genes indicates that the transformation of the proteinase gene into the novel ice-binding protein gene occurred quite recently, about 5–14 million years ago (mya), which is highly consistent with the estimated times of the freezing of the Antarctic Ocean at 10–14 mya, and of the main phyletic divergence of the AFGP-bearing notothenioid families at 7–15 mya. The notothenioid trypsinogen to AFGP conversion is the first clear example of how an old protein gene spawned a new gene for an entirely new protein with a new function. It also represents a rare instance in which protein evolution, organismal adaptation, and environmental conditions can be linked directly.

The abstract above on its own blows your cretinous assertion out of the water, but there's more:

Members of a single teleost suborder, Notothenioidei, overwhelmingly dominate the fish fauna of the freezing (−1.9°C) coastal regions of the Antarctic Ocean in terms of number of species (>50%) (1–3) and biomass (90–95%) (4, 5). Their vast ecological success is linked to ensured survival by the presence of special blood-borne antifreeze glycoproteins (AFGPs; ref. 6). Antifreeze proteins prevent freezing of the body fluids of teleosts, whose equilibrium freezing point (−0.7 to −1°C) is significantly higher than that of seawater (−1.9°C), by adsorbing to small ice crystals in the body and inhibiting their growth (6–9). Besides AFGPs, there are three other structurally different types of antifreeze proteins from various polar and subpolar fishes (10, 11), suggesting that these unique proteins evolved independently at least four times. How these unique proteins evolved in these fishes has remained one of the most important but unanswered questions in the area of antifreeze research. The notothenioid AFGPs exist as a family of at least eight isoforms of different sizes all composed of a simple glycotripeptide repeat, (Thr-Ala/Pro-Ala)n, with the disaccharide galactose-N-acetylgalactosamine attached to each Thr (6, 10), and the dipeptide Ala-Ala at the N terminus.

The authors continue with this:

Notothenioid AFGP Gene Structure.

The complete structure of the AFGP gene from one of the characterized clones, Dm1A (accession no. U58944U58944), and the structure of the 5′ and 3′ AFGP cDNAs (accession nos. U58867U58867, U58868U58868) are depicted in Figs. 1 A and B, respectively. The AFGP polyprotein coding region (2129 nt) in the Dm1A AFGP gene contains 41 copies of AFGP coding sequences that encode four different sized isoforms, linked in tandem by the conserved three-residue spacer, LIF or LNF, similar to that reported for the Nc-AFGP gene from the related N. coriiceps (13). Immediately 5′ to the AFGP coding region is a long stretch of repetitive gt sequences (gt20), which was assigned as part of the presumptive signal peptide in the Nc-AFGP gene (14). However, comparing the AFGP gene and cDNA sequences (Fig. 1 A and B) established that the (gt)n-region in fact comprises the 3′ end of the single intron (I1), which is 1879 nt in length in Dm1A and which intervenes at the C terminus of the true signal peptide encoded in exon 1 (Fig. 1A). Exon 1 encodes the 5′ UTR (27 nt) and most of the signal peptide (40 nt, encodes 13 amino acids). Exon 2 encodes the rest of the signal peptide (six residues by assigning the putative cleavage site right before the AFGP tripeptide repeats begin), the AFGP polyprotein, and the 3′ UTR. The 3′ UTR sequence is 97% identical to that of the Nc-AFGP gene.

The authors then move on to this:

Alignment of Notothenioid AFGP and Trypsinogen Genes.

Alignment of the four notothenioid AFGP and trypsinogen gene and cDNA structures showed three regions of sequence identity between the two genes (Figs. 1 A–D). First, exon 1 (5′ UTR and signal peptide) of the AFGP gene and trypsinogen gene are 94% identical in sequence. Thus, the AFGP gene utilizes the 5′ UTR and signal peptide coding sequence of the trypsinogen gene. Second, the 3′ end region of AFGP gene starting from the penultimate codon through 3′ UTR (255 nt) is 96% identical to the last exon (E6) of trypsinogen gene. Thus, the AFGP gene utilizes trypsinogen E6 as 3′ UTR. Third, the entire trypsinogen intron 1 (238 nt) is present as two segments within the single AFGP intron with an overall sequence identity of 93%. The first 12 nt of trypsinogen I1 inclusive of 5′ splice site correspond to the same in AFGP I1, and the remaining 226 nt inclusive of 3′ splice site and a (gt)36 sequence right before the 3′ splice site correspond to the (gt)20-bearing 3′ end of AFGP I1. Thus, AFGP gene intron 1 is the same as trypsinogen gene I1 plus a large (1.7-kbp) insertion. Immediately 3′ to the (gt)36 sequence in the trypsinogen gene and straddling the splice junction of I1 and E2, a 9-nt element, acagcggca (splice sequence in italics) is found that translates into Thr-Ala-Ala (Fig. 1D and Fig. 2), the building block of the repetitive tripeptide sequence of AFGP. The nucleotide sequence of the three regions of sequence identity between the two genes are shown in Fig. 2. The trypsinogen/AFGP hybrid gene structure is found to be present in the extant AFGP genes of the notothenioids as shown by the multiple AFGP-positive bands on a Southern blot of PCR-amplification products from the genomic DNA of three different notothenioids using the common trypsinogen/AFGP 5′ UTR (cTryp-AF5′) and 3′ UTR (cTryp-AF3′) primers (Fig. 3) and hybridized to an AFGP-specific probe that contains only (Thr-Ala-Ala)n coding sequence.

Moving on to the discussion, we have:


Given the common sequence elements between notothenioid trypsinogen and AFGP genes, and the occurrence of a Thr-Ala-Ala coding element in the trypsinogen gene, the primordial AFGP gene could have risen from an ancestral trypsinogen gene by a combined process of partial gene recruitment and de novo amplification depicted in Fig. 4. E1 (5′ UTR and signal peptide), I1, and several nucleotides of trypsinogen E2 inclusive of the 9-nt Thr-Ala-Ala coding element were recruited to form the 5′ portion of the AFGP gene. A deletion removed the rest of trypsinogen E2 through I5, linking E6 inclusive of the 3′ UTR to the 9-nt Thr-Ala-Ala coding element, and de novo amplification of the coding element gave rise to an entirely new coding region that encodes the repetitive tripeptide backbone of AFGP. The deletion, recruitment, and amplification events did not need to occur in the order given. Indeed, an AFGP/trypsinogen hybrid protein coding region formed by some amount of duplication of the 9-nt Thr-Ala-Ala coding element before bulk deletion of trypsinogen sequence might in fact be a more stable structure for the evolving gene than large deletion first and amplification later. In any case, these DNA rearrangement and amplification events together led to a frameshift resulting in a termination codon (tga) at the start of the recruited trypsinogen E6, and converting it into the penultimate codon that encodes the last amino acid, Gly (ggg; 1 g from splice sequence, 2 from E6) and the 3′ flanking region (or 3′ UTR) of the new gene (Fig. 4). The same penultimate codon (ggg) is found in all notothenioid AFGP genes sequenced (refs. 13 and 14; Fig. 2).

The initial duplication of the 9-nt Thr-Ala-Ala coding element could be a result of slippage replication (16) at the repetitive (gt)n sequence immediately upstream during DNA replications, causing the Thr-Ala-Ala coding element to be copied more than once. Subsequent amplifications could occur through slippage replication or unequal crossing over (17, 18) of the new duplicants. Evidence for amplification of the trypsinogen Thr-Ala-Ala coding element to give rise to the repetitive AFGP polyprotein coding sequence is provided by a striking correspondence between its nucleotide sequence, aca(Thr)-gcg(Ala)-gca(Ala), and those of the tripeptide repeats in extant AFGP genes. In the Dm1A AFGP gene, the preponderance of aca in coding Thr (137/170, 81%), and gca in coding the second Ala (162/171, 95%) strongly indicates that they are duplicants or descendants of the ancestral trypsinogen codons. The first Ala in the tripeptide is coded mostly by gct (65/107, 61%) and the remainder by gcg (38/107, 36%). It is likely that gct, rather than gcg, was the codon for the first Ala in the ancestral trypsinogen Thr-Ala-Ala coding element. Nucleotide substitutions at this codon led to either no change in the amino acid (gct to gcg, Ala), or a Pro for Ala replacement (gct to cct) observed at this Ala position in the antifreeze protein. The occurrence of the latter (gct to cct) is supported by the almost exclusive use of cct in coding the Pro (63/64, 96%) in the Thr-Pro-Ala repeats in the Dm1A gene, as well as in other characterized notothenioid AFGP genes (13, 14).

The authors continue with:

Deciphering the evolutionary process of notothenioid AFGP gene from a trypsinogen gene was made possible by the high degree of nucleotide identities (93–96%) in both the coding and noncoding sequences between the two genes, as well as the close correspondence between the candidate 9-nt ancestral Thr-Ala-Ala coding element in trypsinogen gene and the repetitive AFGP tripeptide coding sequences, all of which indicate that the trypsinogen to AFGP conversion was a recent event. The small divergence (7%) between AFGP and trypsinogen intron 1 sequences particularly supports the recent evolution of the notothenioid AFGP as intron sequences are under no constraint to remain conserved. There are no definitive nuclear gene sequence divergence rates for teleosts available in the literature to estimate the time of divergence between notothenioid trypsinogen and AFGP genes. Using teleost (salmon) mitochondrial DNA divergence rates, 0.5–0.9% per million years (myr; ref. 19), the 4–7% sequence divergence between the two notothenioid genes translates into a divergence time of about 5–14 myr. Evolution of AFGPs at 5–14 million years ago (mya) is remarkably consistent with the estimated mid-Miocene (10–14 mya) time frame during which the Antarctic Ocean cooled to freezing based on paleotemperatures inferred from oxygen isotopic ratios of sea bottom planktonic deposits (20–22). It is also highly consistent with the molecular phylogeny of notothenioids based on mitochondrial 12S and 16S ribosomal RNA gene sequences, which places the main phyletic divergence of the five AFGP-bearing notothenioid families at about 7–15 mya (23). These time frames are not entirely definitive, since paleoceanographic temperatures derived from oxygen isotopic methods were subject to different interpretations, and hypotheses of phyletic relationships among notothenioids differ depending on whether morphological or molecular data are subject to cladistic analysis (3, 23). However, since the driving force for AFGP evolution came from the onset of freezing conditions in the Antarctic waters, and emergence of AFGPs undoubtedly enabled the phyletic radiations of the benthic ancestral notothenioids stock (3) into ice-laden pelagic and surface habitats where they reside today, it is reasonable to expect that the chronology of these three events would overlap. The remarkable agreement in the estimated Miocene times of AFGP gene evolution in this study, the freezing of the Antarctic Ocean inferred from paleoceanographic studies (20–22), and the main phyletic divergence of notothenioids based on molecular phylogeny (23) argue strongly that this time frame could not be due to mere coincidence, but is, in fact, reliable.

A pertinent question is why a pancreatic enzyme protein gene was selected for conversion to the new ice-binding protein. The intestinal fluids of Antarctic notothenioids are known to contain high concentration of AFGPs (24) which serve to inhibit the growth of ice crystals that inevitably enter through food and seawater ingestion (9, 24). Conversion of an existing pancreatic enzyme gene into AFGP gene and expressing it in the pancreas is both positionally and temporally logical as AFGPs thus could reach the digestive tract, simultaneously with pancreatic enzymes, to prevent the intestinal fluid from freezing while the enzymes perform digestive functions. AFGPs continue to be expressed in the notothenioid pancreas today as verified by the production of AFGP cDNAs by RT-PCR amplification of pancreatic mRNA in this study, and the expression appears to be at high levels as indicated by the high intensity of hybridization to an AFGP-specific probe on a Northern blot of pancreatic mRNA (data not shown). It is possible that the notothenioid AFGP gene evolved and became expressed in the pancreas first to protect the intestinal fluid, as it was readily susceptible to freezing through daily intake of ice-associated food or seawater, and later, the expression extended to the liver, which became the synthetic site to provide circulatory antifreeze (25) for freezing avoidance in other extracellular fluid compartments.

The elucidation of how a notothenioid pancreatic trypsinogen gene was transformed into an AFGP gene provides the first clear and plausible evolutionary process by which one of the four known types of antifreeze proteins arose. The antifreeze peptides (type II AFPs) from the sea raven, herring, and smelt share partial protein sequence identity with the carbohydrate recognition domain of C-type lectins or similar domains in lectin-like proteins from other organisms, suggesting evolutionary relatedness (26). Lectins in type II AFP-bearing fishes have not been characterized, and if they indeed gave rise to the type II AFPs in these fishes, it would represent an example of gene recruitment and expression of the same or a very similar protein to perform a different function, much like the recruitment of cellular enzyme genes such as lactate dehydrogenase and others, and express them at high levels to form the lens crystallins (27–30). Evolution of notothenioid AFGP genes represents another evolutionary innovation—recruitment of segments of an existing protein gene plus de novo amplification of a short DNA sequence to spawn a novel protein with a new function. Despite the apparently recent notothenioid AFGP gene evolution, powerful environmental selectional pressure—that is, the threat of freezing death once the Antarctic water reached perennial freezing temperatures—may have driven rapid intragene and whole gene duplications. These processes could readily occur for simple repetitive sequences like the AFGPs, leading to the large AFGP polyprotein gene families we see today.

Oh look, the authors provide evidence for the requisite hypothesis, that Antarctic Notothenioid ice fishes acquired their antifreeze glycoproteins via duplication of a pancreatic trypsinogen gene, and subsequent modification by mutation of the duplicated copy. And, they provide what is effectively a genetic audit trail for the process, allowing the ancestral gene to be reconstructed. Which should not be possible if creationist assertions are something other than the products of their rectal passages.

However, there's another set of evolutionary developments worth covering in detail, and that's the loss of eyes in cave dwelling members of Astyanax mexicanus. This is going to be a substantial exposition, so be patient.

Eye evolution is one of those vexed topics that continues to resurface on forums such as this, and indeed, will probably continue to resurface, courtesy not only of the wilful ignorance (not to mention ideologically motivated discoursive duplicity) of critics of evolutionary theory (Darwin quote mines, anyone?), but because incredulity still persists with respect to this topic. Therefore, I thought it apposite to collect, in one place, as large a body of scientific work on eye evolution, with reference to as many relevant scientific papers as possible, that can be fitted into the confines of posts within these forums. Among those papers are a brace of papers on blind cave fishes, which are particularly apposite with respect to eye evolution, and the illumination of relevant processes and relevant genes.

Having engaged in a literature search on the Mexican Blind Cave Characin, Astyanax mexicanus, for another thread elsewhere, I thought I would bring the material over here, as it makes compelling reading. I found several interesting papers, and provide links to those that can be downloaded in full, and quotes from abstracts where appropriate in order to highlight specific points. Where possible, I shall also provide detailed exposition of the contents of some papers. As a consequence, this is going to be a long post. :)

Basically, the development of the eye in Astyanax mexicanus is controlled by the genes Pax6, shh and twhh among others, though these are, thus far, the ones principally implicated. I suspect that somewhere along the lines, a linkage with HOX genes and possibly even bmp signalling may prove to be part of the total picture once the requisite research is performed - it wouldn't surprise me if this was the case, given how HOX genes and bmp signalling turn up in a diverse range of other developmental mechanisms, but for now, shh and twhh appear to be the prime movers signalling wise.

So, on to the papers! First ...

Evidence for Multiple Genetic Forms With Similar Eyeless Phenotypes In The Blind Cavefish, Astyanax mexicanus by Thomas E. Dowling, David P. Martasian and William R. Jeffery, Molecular Biology & Evolution, 19(4): 446-455 (2002), which can be downloaded in full and read at leisure as a PDF document from [here, and the abstract reads thus:

A diverse group of animals has adapted to caves and lost their eyes and pigmentation, but little is known about how these animals and their striking phenotypes have evolved. The teleost Astyanax mexicanus consists of an eyed epigean form (surface fish) and at least 29 different populations of eyeless hypogean forms (cavefish). Current alternative hypotheses suggest that adaptation to cave environments may have occurred either once or multiple times during the evolutionary history of this species. If the latter is true, the unique phenotypes of different cavedwelling populations may result from convergence of form, and different genetic changes and developmental processes may have similar morphological consequences. Here we report an analysis of variation in the mitochondrial NADH dehydrogenase 2 (ND2) gene among different surface fish and cavefish populations. The results identify a minimum of two genetically distinctive cavefish lineages with similar eyeless phenotypes. The distinction between these divergent forms is supported by differences in the number of rib-bearing thoracic vertebrae in their axial skeletons. The geographic distribution of ND2 haplotypes is consistent with roles for multiple founder events and introgressive hybridization in the evolution of cave-related phenotypes. The existence of multiple genetic lineages makes A. mexicanus an excellent model to study convergence and the genes and developmental pathways involved in the evolution of the eye and pigment degeneration.

Other interesting papers include:

Genetic Analysis of Cavefish Reveals Molecular Convergence in the Evolution of Albinism by Meredith E. Protas, Candace Hershey, Dawn Kochanek, Yi Zhou, Horst Wilkens, William R. Jeffery, Leonard I. Zon, Richard Borowsky and Clifford J. Tabin, Nature Genetics, 38(1): 107-111 (January 2006) which can be downloaded in full from here;

Hedgehog Signalling Controls Eye Degeneration in Blind Cavefish by Yoshiyuki Yamamoto, David W. Stock and William R. Jeffery, Nature, 431: 844-847 (19 July 2004) (not a free download but the abstract is online).

From the latter paper about Hedgehog signalling, I provide the abstract:

Hedgehog (Hh) proteins are responsible for critical signalling events during development but their evolutionary roles remain to be determined. Here we show that hh gene expression at the embryonic midline controls eye degeneration in blind cavefish. We use the teleost Astyanax mexicanus, a single species with an eyed surface-dwelling form (surface fish) and many blind cave forms (cavefish), to study the evolution of eye degeneration. Small eye primordia are formed during cavefish embryogenesis, which later arrest in development, degenerate and sink into the orbits. Eye degeneration is caused by apoptosis of the embryonic lens, and transplanting a surface fish embryonic lens into a cavefish optic cup can restore a complete eye. Here we show that sonic hedgehog (shh) and tiggy-winkle hedgehog (twhh) gene expression is expanded along the anterior embryonic midline in several different cavefish populations. The expansion of hh signalling results in hyperactivation of downstream genes, lens apoptosis and arrested eye growth and development. These features can be mimicked in surface fish by twhh and/or shh overexpression, supporting the role of hh signalling in the evolution of cavefish eye regression.

So it transpires that if you transplant an embryonic lens taken from a surface-dwelling Astyanax mexicanus with normal eyes into the optic cup of an embryonic blind cavefish, normal eye development resumes. Interesting is it not? And, by manipulating the shh and twhh gene expression in surface-dwelling eyed fishes during embryonic development, the scientists were able to reproduce the eye apoptosis seen in the cave dwelling fishes.

An additional paper (downloadable in full from here) is this one:

Early and Late Changes in Pax6 Experession Accompany Eye Degeneration During Blind Cavefish Development by Allen G. Strickler, Yoshiyuki Yamamoto and William R. Jeffery, Development, Genes & Evolution, 211(3): 138-144 (March 2001)

in which the role of the Pax6 gene (which is common to eye development across a wide range of organisms) is examined with respect to the differences in development between the surface-dwelling form of Astyanax mexicanus and the cave-dwelling forms.

From here, you can download the following paper:

Eyed Cave Fish In A Karst Window by Luis Espinasa and Richard Borowsky, Journal of Cave and Karst Studies, 62(3): 180-183 (2000)

which describes the co-existence of eyed and eyeless forms in a cave with a karst window, and the abstract makes VERY interesting reading indeed - namely:

We considered four hypotheses for the origin of Caballo Moro eyed cave fish. The RAPD data rule out that the mixed population represents a transitional stage of evolution, or that the eyed fish are unmodified surface immigrants. We cannot rule out that the eyed fish are the direct descendants of surface fish that have acquired markers from blind fish by hybridization, although the apparent distinctness of the two sub-populations suggests otherwise. An alternative hypothesis, that the eyed fish of the cave are direct descendants of blind cave fish that re-acquired eyes with the opening of the karst window, is consistent
with the data and tentatively accepted.

So here, we have the first cited evidence that when a blind cave population was, by a serendipitous accident, granted readmission to daytime light sources, some of the blind cave fishes regained their eyes over time.

Indeed, I'll cover this paper in more detail, as it makes interesting reading to put it mildly. The paper opens as follows:

Caballo Moro, a karst window cave in northeastern Mexico, supports a mixed population of cave Astyanax mexicanus : eyed and eyeless. The relationships of these sub-populations to one another and to other populations of Mexican tetras were examined using RAPD DNA fingerprint markers. The eyed tetras of Caballo Moro Cave are genetically closer to blind tetras from Caballo Moro and other caves in the region than they are to eyed tetras from the surface. The two forms are not genetically identical, however, and may represent distinct sub-populations.

Eyed and eyeless fish have a distributional bias in the cave, with eyed fish preferentially in the illuminated area and blind fish in the dark zone. Aggression of eyed towards blind fish in the illuminated area contributes to this bias and may serve to stabilize the eye-state polymorphism.

We considered four hypotheses for the origin of Caballo Moro eyed cave fish. The RAPD data rule out that the mixed population represents a transitional stage of evolution, or that the eyed fish are unmodified surface immigrants. We cannot rule out that the eyed fish are the direct descendants of surface fish that have acquired markers from blind fish by hybridization, although the apparent distinctness of the two sub-populations suggests otherwise. An alternative hypothesis, that the eyed fish of the cave are direct descendants of blind cave fish that re-acquired eyes with the opening of the karst window, is consistent with the data and tentatively accepted.

So, there exists a cave in Mexico called Caballo Moro, that has a karst window admitting light, and within this cave, within reach of the light admitted by the karst window, there is a population of Astyanax mexicanus. This population contains fishes that have lost their eyes, conforming to the phenotype that was once described via the taxon Anophthichthys jordani, that taxon now recognised as a junior ynonym of Astyanax mexicanus. However, the population contains fishes with functioning eyes. It is tempting to think that the eyed fishes are members of a surface-dwelling population that have become intermingled with the cave fishes, and, courtesy of still having access to light, retained their eyes. The population genetics of Astyanax mexicanus have been extensively studied, and as a consequence, a great deal is known about the surface-dwelling and cave-dwelling populations of these fishes, including the fact that there exist distinct genetic markers for distinct populations, allowing scientists to alight upon the fact that the eye-loss phenotype has arisen in multiple separate populations independently, via a range of acquired mutations. The relevant paper containing evidence for this is one I've already cited above, namely:

Evidence For Multiple Genetic Forms With Similar Eyeless Phenotypes In The Blind Cavefish, Astyanax mexicanus by Thomas E. Dowling, David P. Martasian and William R. Jeffery, Molecular & Biological Evolution, 19(4): 446-455 (2002)

I'll leave that paper aside for the moment, as I've dealt with it elsewhere in the past, and can always return to it in detail in another post. However, that paper establishes that different cave populations of Astyanax mexicanus possess an eyeless phenotype arising via different sets of mutations in the genes responsible for eye development (namely Pax6, shh and twhh, about which I have posted in the past, including the paper covering Pax6 as a master gene in eye development). Likewise, populations of the surface dwelling eyed phenotype have genetic markers identifying them as belonging to particular populations, where those populations experience little or no gene flow with other populations, and consequently, the provenance of a fish can be determined with reasonable precision by appropriate genetic analysis. The authors of the paper I am covering here have established that the eyed phenotype fishes in the Caballo Moro karst window cave possess genetic markers identifying them as having derived from ancestral eyeless stock. Which means that these fishes had eyeless ancestors, and consequently regained functioning eyes once light was present.

So, it remains to cover the present paper in more detail, and examine the evidence presented therein. Let's do that shall we?

The Mexican Tetra, Astyanax mexicanus, is a visually orienting, schooling fish widely distributed in surface streams of northern Mexico. In addition to the epigean populations, numerous cave forms of this species occur in the Sierra de El Abra region of northeast Mexico (Fig. 1; Mitchell et al. 1977). In contrast to the surface fish, these troglobitic forms have rudimentary, non-functional eyes, and their melanin pigmentation is reduced or absent.

Generally, caves with troglobitic Mexican tetras do not contain eyed tetras, except for the occasional doomed individual swept underground. One exception is El Sótano de El Caballo Moro, which contains an apparently stable, mixed population of A. mexicanus, both eyed and eyeless.

The entrance of Caballo Moro Cave (CMC) is a karst window. Karst windows are habitats within cave systems that are exposed to light, and typically result from cave passage collapse. The 50-m deep entrance pit of CMC is found at the bottom of a 60-m doline, and leads directly to a large “lake” of approximately 18 m x 90 m. (Cave “lake” in this case, is a wide stream pool). Light reaches only the upstream half of the lake, while the downstream half remains in darkness. The lake contains both blind depigmented and eyed pigmented forms of A. mexicanus. The distribution of fish in the lake appears to be biased, with over-representations of blind fish in the dark area and eyed fish in the light area.

Mitchell et al. (1977) observed that the source of the eyed fish of Caballo Moro cave was a mystery. The cave’s entrance pit is 11 km away from the nearest potential resurgence and does not capture a surface stream. Furthermore, there is no permanent water nearby. The nearest recorded surface fish locality in the Río Boquillas system is 4 km distant. They hypothesized that seasonal flooding of Río Boquillas tributaries affords occasional access to the cave through, as yet undetected, sinks.

As part of a larger study of the evolutionary history of the Mexican cave tetra, we investigated the relationships of the eyed fish of CMC. If they represent an unmodified surface population recently captured from a nearby sink, their presence in the karst window would be unremarkable. If, on the other hand, the population were of long standing, it would raise the question of the maintenance of its integrity in the face of potential hybridization with, and introgression of genes from, the troglobites. Alternatively, if the eyed fish of the cave originated from blind cave progenitors, they would make a good model for study of the effects of the reversal of selection pressures on populations.

And thus, the groundwork is laid for what follows. Namely, that there is no obvious source of eyed fishes from surface or epigean populations, with the cave running for 11 Km underground, without capturing a surface stream between the cave's entrance pit and the karst window illuminating the population of interest. Moreover, the nearest population of epigean fishes is 4 Km distant from the cave, and there is no obvious connection between the body of water containing that epigean population, and the mixed population of fishes in the karst window lake, which comprises a mixture of epigean and hypogean (cave-phenotype) fishes. So, the possibilities are:

[1] The epigean phenotype fishes (possessing pigmentation and functional eyes) are a recent arrival, courtesy of an as yet unknown connection between the cave system and a surface body of water supplying these fishes;

[2] The epigean phenotype fishes have coexisted with the hypogean phenotype (eyeless and depigmented) fishes for an extended period of time with little or no interbreeding;

[3] The epigean phenotype fishes have arisen from hypogean ancestors.

[1] is considered unlikely by the authors, given the known geography of the cave system, but is required to be ruled out evidentially. [2] poses problems with respect to the appearance of an isolating mechanism between the two phenotypes, given that prior breeding experiments have established that epigean and hypogean fishes are capable of mating and producing offspring. [3], meanwhile, would provide an extremely interesting example of evolution reversing a character change that had previously occurred in these fishes, but requires evidential support before the postulate can be considered valid. So, let's see what the authors discovered upon further analysis! First, the authors outline their experimental procedures:


The relationships among representative surface and cave populations of Astyanax mexicanus from the El Abra region were studied using RAPD data. RAPD (synonymous with APPCR) technique generates a DNA fingerprint from genomic DNA using the polymerase chain reaction (Welsh & McClelland 1990; Williams et al. 1990). RAPD fingerprints are species and population specific and carry significant amounts of taxonomic information (Borowsky et al. 1995).

The following populations were sampled (Fig. 1): caves: Molino, Vasquez, and Caballo Moro: surface: Río Frío, Río Boquillas and Río Comandante. Astyanax aeneus from the Río Granadas, a tributary to the Río Amacuzac, northeast of Taxco, Guerrero, Mexico, were used as the outgroup for phylogenetic analyses. Two individuals each were examined from Molino cave, Vasquez cave, all surface localities, and A. aeneus. Five blind individuals and six eyed individuals were examined from CMC. RAPD amplification procedures followed Borowsky et al. (1995). Two primers were used: Mey7 (5’ggagtaggggatatgatcgatgga3’) and Mey8 (5’cagcaaacagaaaccagtcag3’). Reactions were cycled five times in a Hybaid thermocycler: 94°C for 70 s, 40°C for 5 minutes, and 72°C for 3 minutes, followed by 35 cycles at higher stringency: 94°C for 70 s, 50°C for 1 minute, and 72°C for 90 s. Reaction products were run on 6% polyacrylamide gels (29:1) and silver stained (after Gottlieb & Chavko 1987). RAPD fragment distributions were compared among individuals using a size match criterion. Each uniquely sized band was assumed to be a character, and character states were scored as “present” or “absent.”

Phylogenetic analysis of the data was done using Paup 4.0b2 software (Swofford 1999). Maximum parsimony analysis (character states unordered) was done by bootstrapping the data (1000 replicates) using full heuristic search to produce a 50% majority-rule consensus tree. For analysis of distance (“mean character difference”), neighbor-joining trees were generated from bootstrapped data (1000 replicates) and used to obtain a 50% majority-rule consensus tree.

A supplementary analysis was done using a Monte Carlo procedure to estimate the variance of distances among individuals within and between the sets of eyed and eyeless fish from CMC. Individual phenotypes for distance comparisons were created by sampling, based on the frequencies of bands in each set. Twenty such pairs of phenotypes were generated for each simulation and the calculated distances were used to estimate means and their standard deviations. For this analysis, distances were calculated as the sum of the absolute differences in band frequencies among taxa or individuals divided by the number of bands.

Now, comes the analytical results!


One hundred and fifty-eight bands were scored, of which 127 were variable and of value in distance analysis, and 58 were parsimony informative. The number of bands observed in any individual ranged from 55-69. The raw data matrix presented as table 1, is organized in the style of a “sequence alignment.” As such, it arrays the character states of the outgroup species along the top row (+, -, and “P” for polymorphic). The character states for the other taxa are arrayed below, using “.” to denote state identity with the outgroup, and the other symbols, where different from the outgroup. The data were sorted by character states in the cave fish, putting “-“ towards the left and “+” towards the right. This arrangement makes apparent a series of derived bands shared among all cave fishes or among all individuals of Caballo Moro cave. These synapomorphies imply a closer relationship of the eyed fish of Caballo Moro cave to other cave fish than to epigean fish.

Indeed, the accompanying figure is quite impressive (see Table 1 charting the RAPD bands for the various populations). The Caballo Moro fishes are manifestly members of a well-defined and genetically distinct grouping, exhibit a well-defined clustering of bands from the DNA analysis that are only partially shared with individuals from the Molino and Vasquez caves (the other two cave populations sampled), and there are marked differences between the Río Frío, Río Boquillas and Rio Comandante fishes and those from Caballo Moro.

Moving on:

This implication is supported by both parsimony and distance analyses, which gave essentially the same result: consensus trees with two clusters, one consisting of the epigean populations and the other of the cave populations. The tree produced by distance analysis (Fig. 2) had a little more structure than the one based on parsimony and may be more appropriate for analysis of populations that can hybridize. The relationship of the eyed and blind fish of Caballo Moro cave is strongly supported by a bootstrap value of 0.83 as is the clustering of all fish of Caballo Moro cave with the other cave fish (bootstrap value of 0.82). The tree also shows a clustering of four of the five blind fish within Caballo Moro, which suggests that the eyed and blind fish of the cave may comprise two distinct sub-populations, in spite of their closeness.

The supplemental distance analysis lends some support to these hypotheses. Distances calculated among populations showed the eyed and eyeless fish of CMC to be closer to each other (0.101) than either was to surface fish (0.337 and 0.359, respectively) or to the other blind cave fish (0.253 and 0.240, respectively). The distance between the eyed and eyeless fish of CMC was investigated in more detail by Monte Carlo simulation. The average distance between simulated eyed and eyeless individuals (0.095 ± 0.015) was significantly greater than the average distance between simulated eyed individuals (0.067 ± 0.016, t(38) = 3.83, p < 0.05) or simulated eyeless individuals (0.031 ± 0.012, t(38) = 9.60, p < 0.05). The means and standard deviations of all the distances measured among the real individuals in the two groups are very similar to those in the simulation (between sets: 0.1226 ± 0.0264; eyed: 0.0965 ± 0.0215; eyeless: 0.0513 ± 0.168) and the t values are high (t(38) = 9.60 and t(43) = 3.24), but only the t tests in the simulation are valid.

Of 41 fish collected from Caballo Moro Cave, 21 were eyed and pigmented, and eighteen had eye rudiments completely covered by muscle and scales and were depigmented. Two were intermediate in phenotype. The collection made from the dark side of the lake had eight fish, one with eyes. The collection made from the illuminated side of the lake had seventeen fish, ten with eyes (locations of other specimens had not been recorded). The biased distribution is statistically significant (Fisher’s exact test, p < 0.05). We observed eyed fish nipping and chasing blind fish on the illuminated side, and this behavior may contribute to the distributional bias within the lake.

Basically, the above tests establish that the Caballo Moro fish form a genetically distinct group, and that furthermore, there exists an interesting set of relations between the eyed and eyeless fishes, which closely matches that of a Monte Carlo simulation of the emergence of eyed and eyeless fishes in that group.

With that, it's time to move on to the authors' discussion of their results:


At least four hypotheses could account for the presence of eyed fish in Caballo Moro cave. The first is that the eyed individuals are surface fish recently swept underground. As such, their residency might be short-lived and they would not necessarily be part of the troglobitic population. A second hypothesis is that the eyed fish represent one phenotypic extreme of a variable cave fish population in evolutionary transition towards eyelessness. A third is that they are the descendants of surface fish swept underground that had interbred with the blind fish and acquired their RAPD marker set by hybridization. A fourth is that the eyed fish are descendants of blind, depigmented cave fish that reacquired eyes and pigmentation through an evolutionary process. The reacquisition of eyes and pigment in troglobites reintroduced to light has been suggested before, for karst window populations of the amphipod Gammarus minus (Culver et al. 1995).

We reject the first hypothesis because it predicts that the eyed fish of CMC should be genetically closer to surface fish than to the blind cave fish. Our results showed the opposite to be true; both distance and parsimony analyses clustered the eyed fish of the cave with blind cave fish rather than surface fish. This clustering was well supported by bootstrap analysis (Fig. 2).

What of the second hypothesis? Is the CMC population in transition from an eyed to a blind condition? Wilkens (1988) hypothesized such a situation in the isolated cave populations of the Micos area, to the west of the El Abra. Micos fish have reduced eyes, but the rudiments are better developed than in the cave tetras of the Sierra de El Abra region, and Micos fish are not fully depigmented. Wilkens suggested that the Micos cave tetras are in transition because they are “phylogenetically younger” than other populations of troglobitic Mexican Tetras, and our (unpublished) RAPD data support this contention.

Nevertheless, we think it unlikely that the CMC population is in transition between the eyed and blind conditions, as in the Micos fish. First, Caballo Moro cave is centrally located within the range of other populations of cave tetras, none of which appear to be in a transitional state. Second, the fish of the Micos caves are uniformly intermediate in eye size and pigmentation phenotype according to Wilkens (1988) and our unpublished observations, while most (95%) of the Caballo Moro cave fish fall into two distinct morphological groups — eyes functional versus blind. Thus, any intermediate “transitional” quality of the CMC population exists primarily as a statistical average of two phenotypic extremes.

We cannot yet distinguish between the third and fourth hypotheses: the eyed fish of the cave may have descended from a captured surface population having interbred extensively with the blind fish or it may have descended from blind cave ancestors by reacquisition of eyes and pigment. Both hypotheses predict extensive sharing of character states among eyed and eyeless fish from CMC and might prove difficult to distinguish in practice.

A test based on distance data may be possible. Our results show that the average distance between eyed and eyeless individuals of CMC is significantly greater than the average distances within these sets. A biologically significant genetic distance between the two groups of fish would arise in different ways according to the two hypotheses. Hypothesis three is one of introgressive hybridization, and would view distance as evidence of a mixing process not yet complete. Hypothesis four is one of centripetal evolution and would view distance as a derived state, as one subset splits from the other. Thus, hypothesis three predicts the eyed fish of CMC to be closer than their eyeless companions to the fish of the surface and more distant from the fish of the other caves. Instead, our data show both groups in CMC to be equally far from surface fish and equally far from the other cave fish. Thus, the current data support hypothesis four, but more will be necessary for a definitive test.

The data presented here confirm the status of the CMC population as one worth further study for the light it can shed upon evolutionary processes. Karst windows, in general, should provide unique opportunities to study the effects of the alteration of selective pressures on troglobites and the ecological and evolutionary interactions between troglobitic and surface species.

Now the authors are being appropriately cautious here, with respect to the data that they have obtained, but, that data is more consistent with the hypothesis of the eyed fishes of Caballo Moro having arisen from eyeless ancestors, than it is with competing hypotheses. Which means, if confirmed by more in-depth study involving larger data sets, that the eyed specimens of Astyanax mexicanus resident in the Caballo Moro karst window lake are fishes that have regained functional eyes, courtesy of appropriate mutations being positively selected for in their lineage. It would be interesting to examine the genetic data for the Pax6, shh and twhh genes for these fishes, as, given their known role in the appearance of the eyeless phenotype in other hypogean lineages of Astyanax mexicanus.

Now, aside from the fact that the above refutes wholesale any notion that selection cannot affect the dissemination of particular genes, or shape the inheritance thereof (which as susu.exp has already noted on numerous occasions elsewhere, is based upon a singularly woeful lack of understanding of basic biology - some critics of evolution apparently hasn't heard of meiosis, apart from anything else), the above findings also drive a tank battalion through creationist quote mining of Crow's paper, because here we have an instance of purported 'genetic deterioration' being thrown into full reverse by evolutionary processes, something which creationist assertions about "genomic entropy" claim simply cannot happen. Once again, the real world demonstrates that blind creationist assertion is nothing more than that - blind assertion.

So, looks like the evidence for the active evolution of these fishes is pretty compelling. :)

Meanwhile, it's time to move on from the blind cave fishes somewhat, and concentrate upon Pax6. The papers extant in this area are very interesting. Indeed, as if yet more evidence for the importance of Pax6 was needed, [here is the Ensembl page covering the Pax6 gene and the oculorhombin protein that it codes for. That page notes that the following diseases are caused by mutations in Pax6:

[1] Aniridia type II - partial or complete absence of the iris, absence of the fovea and malformations of the lens (among other structural malformations). Approximately 67% of these defects are familial, and the inheritance mechanism is autosomal dominant;

[2] Peter's Anomaly - the site describes this condition thus:

[quote]Peter's anomaly consists of a central corneal leukoma, absence of the posterior corneal stroma and descemet membrane, and a variable degree of iris and lenticular attachments to the central aspect of the posterior cornea.[/quote]

In other words, more severe eye defects;

[3] Ectopia pupillae - failure of the pupil to be properly centred;

[4] Foveal hypoplasia - failure of the fovea to develop fully during embryogenesis, inheritance again autosomal dominant;

[5] Autosomal dominant keratitis - opacity of the cornea with accompanying vascularisation, often associated with foveal hypoplasia above;

[6] Ocular coloboma - abnormal development of the optic cup and stalk, accompanied by holes appearing in various eye structures;

[7] Bilateral optic nerve hypoplasia - failure of the optic nerve to develop properly, again with autosomal dominant inheritance;

Here's the human Pax6 gene, formatted using my nice Visual Basic applet:


Here's the protein it codes for, again nicely formatted using my applet:

LQ Ochre

(The legend "Ochre" at the end refers to the fact that the gene ends with an Ochre stop codon, TAA - no amino acid is coded for by this codon).

It's instructive to look at some variants for this gene. Here's one associated with Aniridia Type II:


Now already we know something is wrong here because the gene is a different size. But the BIG surprise is what happens when we look at the protein it codes for ...

YR Ochre

Oops. MAJOR malfunction here!

Basically, this mutant form of the gene fails to code for a working protein full stop. The transcription process hits an Ochre stop codon at the third coding triplet.

Furthermore, the extant online gene databases inform me that there are variations as follows associated with Peter's Anomaly:

[1] Substitution of codon triplet for W (tryptophan) replacing G (glycine) at codon position 18 (bp 52-54);

[2] Subsititution of codon triplet for R (arginine) replacing G (glycine) at codon position 26 (bp 76-78);

[3] Substitution of codon triplet for V (valine) replacing D (aspartic acid) at codon position 53 (bp 157-159) - found principally in Japanese human lineages manifesting the disease (ethnospecific), also associated with congenital cataract and foveal hypoplasia in affected individuals;

[4] Substitution of codon triplet for S (serine) replacing P (proline) at codon position 363 (bp 727-729);

So, it looks once again as if real science knows a LOT more about eye evolution than mendacious propagandists for creationist fantasies dare to even imagine it is possible to know.

Meanwhile, I'll also reprise this material - apologies if I repeat citations of papers cited above here:

Adaptive Evolution of Eye Degeneration in the Mexican Blind Cavefish by W. R. Jeffrey, journal of Heredity, 96(3): 185-196 (Jan 2005) - explains how selection is a key factor in the evolution of eye degeneration in cave fishes

Cavefish as a Model System in Evolutionary Developmental Biology by William R. Jeffrey, Developmental Biology, 231:, 1-12 (1 Mar 2001) - contains experimental tests of hypotheses about eye evolution

Hedgehog Signalling Controls Eye Degeneration in Blind Cavefish by Yoshiyuki Yamamoto, David W. Stock and William R. Jeffery, Nature, 431: 844-847 (14 Oct 2004) - direct experimental test of theories about eye evolution and the elucidation of the controlling genes involved

The Master Control Gene For Morphogenesis And Evolution Of The Eye by Walter J. Gehrig, Genes to Cells, 1: 11-15, 1996 - direct experimental test of hypotheses concerning eye evolution including the elucidation of the connection between the Droso gene and eye morphogenesis, and the experimental manipulation of that gene to control eye development

Why cavefish are blind by Natasha .M. Tian & David .J. Price, Bioessays, 27: 235-238 (Mar 2005) - also reports on the connection between the Pax6 and hedgehog signalling genes and how these are subject to selection over time

Let's have a look at some of the contents of those papers shall we?


The evolutionary mechanisms responsible for eye degeneration in cave-adapted animals have not been resolved. Opposing hypotheses invoking neural mutation or natural selection, each with certain genetic and developmental expectations, have been advanced to explain eye regression, although little or no experimental evidence has been presented to support or reject either theory. Here we review recent developmental and molecular studies in the teleost Astyanax mexicanus, a single species consisting of a sighted surface-dwelling form (surface fish) and many blind cave-dwelling forms (cavefish), which shed new light on this problem. The manner of eye development and degeneration, the ability to experimentally restore eyes, gene expression patterns, and comparisons between different cavefish populations all provide important clues for understanding the evolutionary forces responsible for eye degeneration. A key discovery is that Hedgehog midline signaling is expanded and inhibits eye formation by inducing lens apoptosis in cavefish embryos. Accordingly, eyes could have been lost by default as a consequence of natural selection for constructive traits, such as feeding structures, which are positively regulated by Hh signaling. We conclude from these studies that eye degeneration in cavefish may be caused by adaptive evolution and pleiotropy.

Oh dear. The hard evidence from the real world supports evolution. Let's look at the next paper:


The Mexican tetra Astyanax mexicanus has many of the favorable attributes that have made the zebrafish a model system in developmental biology. The existence of eyed surface (surface fish) and blind cave (cavefish) dwelling forms in Astyanax also provides an attractive system for studying the evolution of developmental mechanisms. The polarity of evolutionary changes and the environmental conditions leading to the cavefish phenotype are known with certainty, and several different cavefish populations have evolved constructive and regressive changes independently. The constructive changes include enhancement of the feeding apparatus (jaws, taste buds, and teeth) and the mechanosensory system of cranial neuromasts. The homeobox gene Prox 1, which is expressed in the expanded taste buds and cranial neuromasts, is one of the genes involved in the constructive changes in sensory organ development. The regressive changes include loss of pigmentation and eye degeneration. Although adult cavefish lack functional eyes, small eye primordia are formed during embryogenesis, which later arrest in development, degenerate, and sink into the orbit. Apoptosis and lens signaling to other eye parts, such as the cornea, iris, and retina, result in the arrest of eye development and ultimate optic degeneration. Accordingly, an eye with restored cornea, iris, and retinal photoreceptor cells is formed when a surface fish lens is transplanted into a cavefish optic cup, indicating that cavefish optic tissues have conserved the ability to respond to lens signaling. Genetic analysis indicates that multiple genes regulate eye degeneration, and molecular studies suggest that Pax6 may be one of the genes controlling cavefish eye degeneration. Further studies of the Astyanax system will contribute to our understanding of the evolution of developmental mechanisms in vertebrates.

Oh look. More hard evidence from the real world supporting eye evolution. Namely that:

[1] Different cave fish populations evolved the eye apoptosis mechanism independently, and have different mutations coding for this;

[2] Other senses, particularly those connected with feeding efficiency, are enhanced in the blind cave populations of Astyanax mexicanus, and the underlying genetic mechanism for this is being elucidated, with special reference to the Prox 1 gene;

[3] In embryonic fishes, eye formation begins normally, but then undergoes reversal because of cell apoptosis controlled by signalling from the lens tissues, and experimental transplantation of a normal lens from a sighted embryo into an optic cup belonging to a cave dwelling embryo results in the restoration of normal eye formation;

[4] The genes involved in this process are now known, and the Pax6 gene, which has been demonstrated experimentally to be the master control gene for eye morphogenesis, is involved in the differential formation of eyes in cave dwelling Astyanax mexicanus populations.

However, one of the best papers I can present is this - the very paper that supports the statement I have just made above about the role of Pax6, namely:

The Master Control Gene For Morphgenesis And Evolution Of The Eye by Walter J. Gehrig, Genes To Cells, 1: 11-15, 1996.

I quote:

Abstract. The human aniridia, the murine small eye, and the eyeless mutations of Drosophila affect homologous (Pax-6) genes that contain both a paired- and a homeobox. By ectopic expression of these genes, functional eyes can be induced on the legs, wings and antennae of the fly, indicating that eyeless (Pax-6) is the master control gene for eye morphogenesis. The finding of Pax-6 from flatworms to humans suggests that eyeless is a universal master control gene and that the various types of eyes in the various animal phyla may have evolved from a single prototype.

However, the best part is when we look at the article in detail ...

Hox and Pax genes

Homeotic mutations in Drosophila have led to the isolation of master control genes specifying the body plan. Loss- and gain-of-function mutations in these genes lead to opposite homeotic transformations: in Antennapedia (Antp) for example, loss-of-function mutations lead to the partial transformation of middle legs to antennae, whereas gain-of-function mutations induce the transformation of antennae into middle legs. These transformations in opposite directions suggest that Antp is a switch gene inducing the leg development pathway. We have tested this hypothesis by expressing the normal ANTP protein and asking whether leg structures can be induced in other parts of the body. As predicted, antenna-to-leg transformations can be induced in transgenic flies carrying an Antp cDNA gene under the control of a heat shock promoter (Scheuwly et al., 1987). Heat induction of this transgene during the early third larval stage, just before the antenna becomes determined, leads to the induction of middle legs, indicating that Antp is a master control gene switching on all the genes required for leg morphogenesis. This experiment was the first attempt to redesign the body plan of the fly. Even though the heat shock promoter induces the ANTP protein all over the animal the morphogenetic effect is restricted to the antennae. In the more posterior body segments, Antp has to compete with the homeotic genes of the bithorax complex that specify the more posterior body segments, each segment being specified by a particular combination of homeotic proteins. Hameotic genes are characterised by the homeobox, a 180 bp DNA segment encoding the homeodomain, the DNA binding domain of the respective proteins (McGinnis et al., 1984a,b; Scott & Weiner 1984). The homeotic proteins serve as transcription factors controlling a large number of subordinate genes involved in morphogenesis.

The paired box encodes another DNA binding domain and characterises the Pax genes (see Noll 1993 for review). The Pax genes are a perfect example of what has been called evolutionary tinkering (Jacob 1977). Some Pax genes have a paired box only, some have both a paired and a homeobox, and some have a paired and a partial homeobox. This indicates that in the course of evolution new genes can be generated by putting together bits and pieces from pre-existing genes by recombination, strongly resembling tinkering.

The Pax6 Gene

Using Drosophila probes, a family of mammalian Pax genes has been cloned, including Pax-6 which includes a paired and a homeobox (Walther & Gruss 1991). Subequently it was shown that the murine Small eye (Hill et al., 1991) and the human Aniridia (Ton et al., 1991) mutations affect the respective Pax-6 genes.Mice heterozygous for Small eye (Sey) mutations have reduced eyes, whereas homozygous carriers of the mutation are lethal and lack eyes as well as the nose. The human Aniridia (An) syndrome has a similar phenotype with heterozygotes having reduced eyes sometimes lacking the iris, and a putatively homozygous, lethal foetus lacking eyes completely has also been described. Pax-6 is expressed in the spinal cord, parts of the brain and particularly, at all stages of eye morphogenesis, first in the optic sulcus, then in the optic vesicle, the pigmented and the neural retina, the iris, in the lens and finally in the cornea. This expression pattern led to the suggestion that Sey might control eye induction (Walther and Gruss 1991). The induction of the lens by the optic cup had been demonstrated in frogs by Spemann (1901) and Lewis (1904) who deserve credit for the first experimental documentation of a case of embryonic induction: when the optic vesicle is transplanted under the flank epidermis, an ectopic eye with a lens is induced. However, Spemann and Lewis did not consider the possibility that genes might control eye induction.

On the basis of a comparison between the Pax genes of mammals and Drosophila, Noll (1993) proposed that certain genes are homologous, but no homologue for the mammalian Pax6 gene had been found in Drosophila. This gene was discovered in my laboratory quite accidentally in a control experiment (Quiring et al., 1994). Even though a Pax-6 homologue was expected in Drosophila, it came as a great surprise that mutations in this gene have an eyeless phenotype. The first eyeless (ey) mutation was discovered as early as 1915 by Hoge (Hoge 1915). Homozygous ey mutant flies have strongly reduced eyes or they lack eyes completely. The cloned Pax-6 homologue maps to section 102D on chromosome 4, at the ey locus. In two independent spontaneous mutations, ey(2) and ey(R), the cloned gene carries two different transposon insertions, and in both mutants the cloned gene is neither expressed in the eye primordia of the embryo nor in the eye imaginal discs of the larva, strongly suggesting that the cloned Pax-6 gene represents ey. The transposon insertions disrupt an eye specific enhancer preventing gene expression in the eye primordia. Furthermore, the sequence conservation between the mammalian and insect gene are very high: 95% amino acid sequence identity is found in the paired boxes and 90% between the homeoboxes plus some scattered identity outside of the boxes. Also, two out of three intron splice sites in the paired box, and and one of the two splice sites in the homeobox are conserved, indicating that these genes are true homologues.

This is an unexpected finding since the single lens eye of vertebrates was generally considered to have evolved independently of the compound eye of insects because these two eye types are morphologically completely different. Since homologous organs share variations of the same genetic programme, the possible homology between the insect and the vertebrate eye has to be reconsidered.

Eyeless is the master control gene for eye morphogenesis

The high degree of sequence conservation between ey and Sey or An and the similarity of the mutant phenotypes, as well as the patterns of expression, suggested that these genes play a key role in eye morphogenesis and evolution. However, it was not obvious that they are master control genes since the loss-of-function mutations lead to a loss of eye structures, rather than their homeotic transformation. Thus, the mutational block might occur at the initial steps of the eye development pathway, which is compatible with a possible tole of ey as a master control gene, but it may also occur at a lower level of the hierarchy. This is exemplified by other mutations blocking eye devlopment, like eyes absent, which act downstream of ey. In order to find out whether ey is a master control gene, I planned to construct a gain-of-function mutant and to express the normal EY protein ectopically in other body parts of the fly. The prediction was that the ectopic expression of EY protein would induce ectopic eye structures, if ey were a master control gene. I was encouraged to try out this bold experiment since I knew from transdetermination experiments that wing imaginal disc tissue that is cultured continuously in the abdominal cavity of female flies (Gehrig et al., 1968) can eventually give rise to eye facets (Fig. 2A). This raised the possibility that ey[sup]+[/sup] might induce eye structures at least in wing discs. My collaborators Georg Halder and Patrick Callaerts used both the heat shock vector for ubiquitous expression of ey[sup]+[/sup] (as in the case of Antp mentioned above) and the GAL4 system for targeted gene expression (Brand & Perrimon 1993) by means of enhancer detector strains expressing GAL4 and/or leg and antennal discs. As indicated in Fig. 1, GAL4 drives the expression of an ey(+) gene carrying several GAL4 upstream activating sequences (UAS). By crossing the GAL4 enhancer detection stock with the UAS-ey(+) target gene stock, EY protein can be targeted onto the wing, leg and antennal discs. In contrast to the heat shock vector which requires precise timing of gene expression in relatively short pulses, the GAL4 system allows continuous expression.

As shown in Figs 2B and 3, ectopic eye structures can be induced by switching on the ey(+) c-DNA in the wing and antennal discs, and also in leg discs (Halder et al., 1995). The ectopic eyes are morphologically normal with normal photoreceptors, lens, cone and pigment cells and an electroretinogram as it is typical for photoreceptor cells can be recorded, when the ectopic eyes are exposed to light (P. Callaerts, unpublished data). Thus the formation of an ectopic eye can be induced by switching on a single gene. Therefore, we consider ey to be a master control gene for eye morphogenesis. In addition, ey has other functions in the brain, the nose and the ventral nervous system that remain to be determined.

Oh dear. We know rather more about the genetic processes involved in eye formation and evolution than creationists think. The requisite genes, as I've already established above, are found right across a hole brace of animal phyla from flatworms to mammals, including you and I. And, that knowledge was derived by direct manipulation in the laboratory of the requisite genes, to determine how they work.

One question I've never seen creationists answer with a substantive answer (as opposed to vacuous apologetics) is this: why has their magic man chose to produce cave fishes that have all the genetic and molecular machinery for eye formation, which initiates normal eye development to begin with but then goes into reverse, and moreover exhibit different mutations for this in different populations? If their magic man knew that these fishes were going to end up in caves, why bother giving them the genetic and molecular machinery for eyes in the first place? Bit of a cock up there, creating these fishes in such a manner as to provide evidence for evolution.

Also, I'm reminded of the following video clip (with bonus appearance by Stephen Jay Gould):

Gould On eye evolution

Note that all of the postulated intermediate stages exist in real living organisms today.

I think this should cover all of the relevant scientific bases with respect to eye evolution and the role of specific genes therein.

So, having dealt with that assertion, let's move on ...

Not only that these evolutionary theories completely neglect how the first complete set of DNA information ( contained in the first living cell ) came to exist in the first place


The emergence of the first ancestral genetic sequences is covered more than adequately by the abiogenesis literature, which includes dozens of papers on RNA synthesis and subsequent conversion to DNA. Here's a sample list of papers covering prebiotic RNA synthesis:

Autocatalytic Aptazymes Enable Ligand-Dependent Exponential Amplification Of RNA by Bianca J. Lam and Gerald F. Joyce, Nature Biotechnology, 27(3): 288-292 (March 2009)

Catalysis In Prebiotic Chemistry: Application To The Synthesis Of RNA Oligomers by James P. Ferris, Prakash C. Joshi, K-J Wang, S. Miyakawa and W. Huang, Advances in Space Research, 33: 100-105 (2004)

Cations As Mediators Of The Adsorption Of Nucleic Acids On Clay Surfaces In Prebiotic Environments by Marco Franchi, James P. Ferris and Enzo Gallori, Origins of Life and Evolution of the Biosphere, 33: 1-16 (2003)

Darwinian Evolution On A Chip by Brian M. Paegel and Gerald F. Joyce, Public Library of Science Biology, 6(4): e85 (April 2008)

Emergence Of A Replicating Species From An In Vitro RNA Evolution Reaction by Ronald R. Breaker and Gerald F. Joyce, Proceedings of the National Academy of Sciences of the USA, 91: 6093-6097 (June 1994)

Enzymatic Synthesis Of DNA On Glycerol Nucleic Acid Templates Without Stable Duplex Formation Between Product And Template by Ching-Hsuan Tasi, Jingyang Chen and Jack W. Szostak, Proceedings of the National Academy of Sciences of the USA, 104(37): 14598-14603 (11th September 2007)

Homochiral Selection In The Montmorillonite-Catalysed And Uncatalysed Prebiotic Synthesis Of RNA by Prakash C. Joshi, Stefan Pitsch and James P. Ferris, Chemical Communications (Royal Society of Chemistry), 2497-2498 (2000) [DOI: 10.1039/b007444f]

Mineral Catalysis And Prebiotic Synthesis: Montmorillonite-Catalysed Formation Of RNA by James P. Ferris, Elements, 1: 145-149 (June 2005)

Mineral Surface Directed Membrane Assembly by Martyn M. Hanczyc, Sheref S. Mansy and Jack W. Szostak, Origins of Life and Evolution of Biospheres, 37(1): 67-82 (February 2007)

Montmorillonite Catalysis Of 30-50 Mer Oligonucleotides: Laboratory Demonstration Of Potential Steps In The Origin Of The RNA World by James P. Ferris, Origins of Life and Evolution of the biosphere, 32: 311-332 (2002)

Montmorillonite Catalysis Of RNA Oligomer Formation In Aqueous Solution: A Model For The Prebiotic Formation Of RNA by James P. Ferris and Gözen Ertem, Journal of the American Chemical Society, 115: 12270-12275 (1993)

Montmorillonite-Catalysed Formation Of RNA Oligomers: The Possible Role Of Catalysis In The Origins Of Life by James P. Ferris, Philosophical Transactions of the Royal Society Part B, 361: 1777-1786 (7th September 2006)

Nucelotide Synthetase Ribozymes May Have Emerged First In The RNA World by Wentao Ma, Chunwu Yu, Wentao Zhang and Jiming Hu, The RNA Journal, 13: 2012-2019, 18th September 2007

Prebiotic Chemistry And The Origin Of The RNA World by Leslie E. Orgel, Critical Reviews in Biochemistry and Molecular Biology, 39: 99-123 (2004)

Ribozymes: Building The RNA World by Gerald F. Joyce, Current Biology, 6(8): 965-967, 1996

RNA-Catalysed Nucleotide Synthesis by Peter J. Unrau and David P. Bartel, Nature, 395: 260-263 (17th September 1998)

RNA-Catalyzed RNA Polymerization: Accurate and General RNA-Templated Primer Extension by Wendy K. Johnston, Peter J. Unrau, Michael S. Lawrence, Margaret E. Glasner and David P. Bartel, Science, 292: 1319-1325, 18th May 2001

RNA-Directed Amino Acid Homochirality by J. Martyn Bailey, FASEB Journal (Federation of American Societies for Experimental Biology), 12: 503-507 (1998)

RNA Evolution And The Origin Of Life by Gerald F. Joyce, Nature, 338: 217-224 (16th March 1989)

Self-Sustained Replication Of An RNA Enzyme by Tracey A. Lincoln and Gerald F. Joyce, ScienceExpress, DOI: 10.1126/science.1167856 (8th January 2009)

Single-Molecule Imaging Of An In Vitro Evolved RNA Aptamer Reveals Homogeneous Ligand Binding Kinetics by Mark P. Elenko, jack W. Szostak and Antoine M. van Oijen, Journal of the American Chemical Society, 131: 9866-9867 (2009)

Synthesis Of 35-40 Mers Of RNA Oligomers From Unblocked Monomers. A Simple Approach To The RNA World by Wenhua Huang and James P. Ferris, Chemical Communications of the Royal Society of Chemistry, 1458-1459 (2003)

Synthesis Of Long Prebiotic Oligomers On Mineral Surfaces by James P. Ferris, Aubrey R. Hill Jr, Rihe Liu and Leslie E. Orgel, Nature, 381: 59-61 (2nd May 1996)

Template-Directed Synthesis Of A Genetic Polymer In A Model Protocell by Sheref S. Mansy, Jason P. Schrum, Mathangi Krisnamurthy, Sylvia Tobé, Douglas A. Treco and Jack W. Szostak, Nature, 454: 122-125 (4th June 2008)

The Antiquity Of RNA-Based Evolution by Gerald F. Joyce, Nature, 418: 214-221, 11th July 2002

The Roads To And From The RNA World by Jason P. Dworkin, Antonio Lazcano and Stanley L. Miller, Journal of Theoretical Biology, 222: 127-134 (2003)

Transcription And Translation In An RNA World by William R. Taylor, Philosophical Transactions of the Royal Society Part B, 361: 1689-1702 (11th September 2006)

So, even though my list of papers on this topic is incomplete, I can still bring 27 peer reviewed papers to the table to discuss this topic, and if required, provide detailed expositions thereof. Looks like another of your assertions has just died a death.

Moving on ...

but they also completely neglect the ultimate origin of the underlying design ( like meiotic cell division, fertilization, mitotic cell division, cellular differentiation and morphogenesis ) that even make the transformation of these DNA information into physical plants and animals to be possible.

Again this is bullshit. Oh wait, I have 31 papers covering morphogenesis alone in my collection, including papers devoted to the contribution made to this topic by Alan Turing, and his reaction-diffusion model, which has been used successfully to replicate the emergence of butterfly wing patterns. I'll leave a full exposition of that lot for another time.

Even if we assume that the first living cell managed to evolve from non living materials and again managed to replicate itself ( abiogenesis—a problem that all the world scientists are yet to be solved)

Apparently you are unaware of the literature extant on model protocells and their synthesis. I have 47 papers devoted to this topic in my collection. Which shall I bring here first?

What later caused some of these self-replicating cells to abandon their diploid way of life and suddenly change to become haploid cells (meiotic cell division)—an event that make sexual reproduction to be possible— ?

Oh dear. Apparently you're unaware that the first cells WERE haploid. And that the modern mechanism for sexual differentiation has simpler antecdents, which are still present in yeasts. Which regularly switch between haploid and diploid forms. Shall I bring the full exposition on yeast sex here for you to read?

What later caused two of these haploid cells to start fusing with one another during sexual reproduction in order to restore their original diploid state ( fertilization)

The same mechanisms that drove endosymbiosis?

What later caused this fused cell (called zygote) to multiply and form a compact ball of similar cells (mitotic cell division) ?

Apparently you're unaware of the experimental recreation of mulicellularity from a single celled ancestor documented in this paper:

Phagotrophy By A Flagellate Selects For Colonial Prey: A Possible Origin Of Multicellularity by Martin.E. Boraas, Dianne.B. Seale and Joseph .E. Boxhorn, Evolutionary Ecology 12(2): 153-164 (February 1998 ) [Full paper downloadable from here]

Let's take a look at the contents of this paper shall we?


Predation was a powerful selective force promoting increased morphological complexity in a unicellular prey held in constant environmental conditions. The green alga, Chlorella vulgaris, is a well-studied eukaryote, which has retained its normal unicellular form in cultures in our laboratories for thousands of generations. For the experiments reported here, steady-state unicellular C. vulgaris continuous cultures were inoculated with the predator Ochromonas vallescia, a phagotrophic flagellated protist (`flagellate'). Within less than 100 generations of the prey, a multicellular Chlorella growth form became dominant in the culture (subsequently
repeated in other cultures)
. The prey Chlorella first formed globose clusters of tens to hundreds of cells. After about 10-20 generations in the presence of the phagotroph, eight-celled colonies predominated. These colonies retained the eight-celled form indefinitely in continuous culture and when plated onto agar. These self-replicating, stable colonies were virtually immune to predation by the flagellate, but small enough that each Chlorella cell was exposed directly to the nutrient medium.

Take a look at that. A previously unicellular organism, that had remained unicellular for thousands of generations, became multicellular when a predation selection process was applied, and retained its new, multicellular form whilst subject to said predation. Moreover, the process eventually stabilised at the colony size that was optimally balanced between resistance to predation and access to surrounding nutrients in its aquatic environment.

The transition from unicellularity to multicellularity is the first postulated step in the process leading to the production of new phyla. This process has been experimentally observed, as the above paper documents. The experiments in question are reliably repeatable with any Chlorella vulgaris colony.

Let's take a look at the paper in detail, shall we?


Predation may have played a pivotal role in promoting increased diversity in primordial communities. Stanley (1973) used ecological theory to address an important enigma in palaeontology: the explosive diversification of organisms at the boundary of the Cambrian, around 2 × 10[sup]9[/sup] years after life originated. On the one hand, the long duration of the exclusively prokaryotic period implies that the process triggering the diversification was a unique event with an extremely low probability. On the other hand, even the scanty fossil record clearly demonstrates a rapid proliferation of new, multicellular organic forms. Stanley (1973) suggested an ecological mechanism: the origin of phagotrophy (ingestion of whole prey). He reasoned that single-celled organisms of the Precambrian were resource-limited, with a few species saturating the relatively homogeneous and limited nutrient pool available. Before phagotrophy, prevalent selection pressures among Precambrian phototrophs were for effcient nutrient competition (e.g. a high surface-to-volume ratio provided by small cell size). However, with the advent of phagotrophy, resistance from this new mortality factor became a novel selective pressure for the phototrophs, possibly selecting for multicellularity. Both herbivorous and carnivorous protists arose virtually simultaneously, which may have triggered `self-propagating feedback systems of diversification' and the rapid proliferation of multicellular forms (Stanley, 1973). On the basis of ecological studies showing an association between `cropping' and more diverse communities, Stanley (1973) argued that the `sudden proliferation of complex food webs formed by taxa invading previously vacant adaptive zones produced an explosive diversification of life over a period of a few tens of millions of years'.

Analyses of adaptive trends in living prey populations or patterns of diversity in the fossil record are critical in proposing mechanisms for trends in early evolution (Hanson, 1977). Such analyses support an hypothesis of predation as an important factor in escalating rates of evolution (Vermeij, 1987) and in leading to multicellularity (Bonner, 1988). In addition, `arms-race' hypotheses argue that an adaptive change by one species (usually the prey) in an interaction can select for development of a counter-adaptation by another species (usually the predator), leading to continuous evolution within the interacting species (Van Valen, 1973; Dawkins and Krebs, 1979). Data from
palaeontological studies necessarily are correlative, so experiments also are needed to establish the relative selective power of predation as an evolutionary mechanism for prey morphology shifts.

In this paper, we document an experimental system where predation by a phagotrophic protist (Ochromonas vallescia) resulted in the rapid proliferation of a predator-resistant multicellular prey from within a population of algae (Chlorella vulgaris).

Oh look. Once again, we see the establishment of new trophic niches as a driving factor in speciation. As has been observed elsewhere with, for example, Rhagoletis pomonella, a Dipteran insect that underwent a speciation event as a result of trophic migration (switching to a new larval food supply) followed by assortative mating amongst the resulting adults. In the case of this insect, the original population extant in North America fed upon hawthorn fruits, but upon the introduction of apple trees by humans, some of these insects switched to apples. Those insects that switched to apples assortatively mated, only mating with other apple-feeding members of the population, and likewise, those insects that remained feeding upon hawthorns only mated with other hawthorn-feeding insects. Thus an behavioural isolation barrier preventing gene flow between the two populations arose, and the two populations diverged to the point of producing an incipient speciation event. The parasites that attack Rhagoletis pomonella are also exhibiting the same divergence: those parasitising apple-feeding fly larvae do not interbreed with those parasitising hawthorn-feeding fly larvae, which means that trh trophic migration of some individuals of Rhagoletis pomonella is driving sympatric speciation in several different insect species. But I digress, and need to return to papers on Rhagoletis pomonella at a later stage. Let's continue with Boraas and the Chlorella experiments in the meantime:

Materials and methods

Culture system and organisms

Organisms were maintained in continuous culture using the same chemostat systems we have used routinely in our laboratories to maintain axenic cultures of unicellular Chlorella since 1974 (Boraas, 1979, 1983). A single custom-blown glass culture tube (volume constant at 500 ml) was held under constant conditions of light (c. 100 μEinsteins) and temperature (25 ± 0:5°C). The nutrient medium, which was held in a large reservoir, was deficient in nitrogen (0.5 mM nitrate), with all other essential elements in excess. Inflow from the medium reservoir into the cultures was held constant, at a flow rate of 0.035 ml per h, with a Harvard peristaltic pump.

Initially, the culture tube was filled with medium and inoculated with Chlorella vulgaris Beij obtained from the University of Texas Culture Collection (UTEX #26). A steady state was established for the alga, which was then available as food to the flagellate predator. In the past two decades, except for rare anomalies (loose clusters of algae seen perhaps two or three times per year), this Chlorella culture has always exhibited its normal unicellular morphology in our routine microscopic screens of our continuous cultures.

We have identi®ed the protist used in these experiments as Ochromonas vallescia (Boraas et al., 1988). The O. vallescia was isolated from a rotifer-Chlorella culture in the laboratory and, presumably, originated from the Milwaukee Harbour (the Center for Great Lakes Studies is situated on the harbour). In culture, this almost spherical Ochromonas had a diameter of 8-15 μm and a minimum doubling time of 6 h.

As an obligate phagotroph (Borass et al., 1988), this Ochromonas requires a constant supply of food. For about 7 years, we have maintained this protist in the second stage of a two-stage chemostat culture, receiving Chlorella as food from the first stage (Boraas et al., 1988, 1992; Holen and Boraas, 1995). In the studies reported here, the flagellate was inoculated directly into the steady-state algal culture, in the first stage. This established a predator-prey culture in which the Chlorella were growing on inorganic nutrients and the Ochromonas were feeding on the Chlorella.

Sampling and observation

Samples were removed by sterilized syringe through a sterilized silicone rubber port in the culture vessel tube (see Boraas, 1983). Numbers, size distributions, and biovolumes of populations of both the alga and the protist were measured in each sample with a Particle Data Celloscope. Each sample was suspended in 0.4% 0.2-μm filtered saline upon collection and processed immediately using a 120-μm aperture at a single setting of aperture current and amplifier gain. We have found that electronic particle counting is a precise, rapid method for obtaining counts, size distributions and biomass estimates for planktonic organisms (Seale, 1980, 1982; Boraas, 1983). Since these size distributions contained both algae and protists, visual verification of the size distributions in the cultures were obtained with a light microscope.

Samples for SEM microscopic examination were preserved in 3% gluteraldehyde at room temperature. Chlorella samples from these vials were prepared for SEM analysis by being washed with distilled water, filtered onto a Nuclepore filter, then critical-point dried in CO2 and sputter-coated with gold. Fresh flagellate SEM samples were fixed in 2% gluteraldehyde in 0.1 M cacodylate buffer, washed twice in distilled water with centrifugation, and then treated as for the Chlorella. Samples for TEM were fixed in 4% gluteraldehyde for 1 h, washed in Milliong's phosphate buffer (pH 7.2) and post-fixed in 2% osmium tetroxide for 1 h, washed twice in buffer and embedded in 1.5% agar at 45°C, dehydrated in acetone and embedded in Spur's epoxy. Sections were stained in lead and uranyl acetate immediately after sectioning. They were viewed with a Hitachi Hu 11B-2 transmission electron microscope.

Interactions between the flagellate predator and algal prey were observed with a video microscopy system (Boraas et al., 1992). The microscope was a Zeiss Standard equipped with a prism trinocular and a C-mount adapter attached to a Dage-MTI model NC-65-SA video camera with a Newvicon imaging tube. Brightfield illumination was used. The output of the video scanner was fed to a Sony model VO-1600 ¾ inch (19 mm) video cassette recorder (VCR), recording at a rate of 30 frames per second.


Morphology and ecology of the predator

We did not detect any obvious changes in either the morphology or the feeding ecology of the predator during this study. The Ochromonas used in this study has two flagella (Fig. 1a,e) and a chloroplast (Fig. 1b-d), typical of the Class Chrysophyceae, genus Ochromonas (Boraas et al., 1988). Chrysophytes, although algae, are often mixotrophic, capable of both photosynthesis and phagotrophy (Holen and Boraas, 1995). Although Ochromonas spp. are usually phototrophic, O. vallescia, despite the chloroplast, is incapable of photosynthesis (Boraas et al., 1988). The long, hispid flagellum is used primarily for locomotion and food-cell capture, whereas the short, naked flagellum is used to manipulate the captured food cell during ingestion, based on our video microscopy studies (Boraas et al., 1992). The flagellates used in this study retained these characteristics.

Sequence of development of multicellular Chlorella

The Chorella seen in the culture before predation was the typical unicell (5-6 μm diameter), with numerous empty mother cells interspersed (see Discussion). As expected from previous studies (Boraas, 1980), in the predator-prey culture, this Chlorella population declined immediately from an initial density of 2 × 10[sup]6[/sup] cells ml[sup]-1[/sup], and the predator population increased to a maximum density. The combined suspended particle size distribution throughout this initial growth phase (0 days in Fig. 2a) showed two distinct peaks: Chlorella unicells with a mean diameter of about 6 μm and O. vallescia with an equivalent spherical diameter of 12 μm (Fig. 2a). After their consumption had reduced the Chlorella, the flagellate population also declined, due to starvation and washout of cells from the culture (5 days, Fig. 2a). This reduction in predation pressure allowed the Chlorella population to recover and increase rapidly, in the manner of a classical predator-prey oscillation. During the recovery of the algal population, an unexpected result was observed: the prey Chlorella now included colonial growth forms as well as unicells (10 days, Fig. 2a). The number of cells per colony ranged from four to hundreds (Fig. 1c), bracketing and masking the flagellate size distribution (Fig. 2a). During a second cycle of flagellate growth and Chlorella decline (16 days, Fig. 2a), the Chlorella colonies persisted while the Chlorella unicells declined to <1% of the total cells in the culture.

After 20 days of mixed-species culture, the Chlorella population had many colonies with more than 20 cells (Figs 1c, 2b). The number of cells per colony then gradually declined to a mode of eight and the system entered a steady state (Fig. 2a,b). Flagellates and Chlorella unicells in this steady state had population densities reduced to about 0.1% of their maximum numbers during the transient phases. The bulk of the biomass in this steady state was in eight-celled Chlorella colonies (Fig. 1d), with a mean colony diameter of approximately 17 μm. The cells in these stable colonies of predated cultures were enclosed within an envelope (Fig. 1d), apparently the mother cell wall of the neonatal cells (see Discussion). Empty mother cell walls were virtually absent from the culture.

The Chlorella colonies were stable and self-replicating. Colonies had variable morphologies, even during the steady-state phase (Fig. 1a,d), but the majority were roughly spherical, usually with eight (but occasionally four) cells per colony. The colonies were photosynthetically active, and reproduced indefinitely as colonies in the light in either chemostat culture or on agar. When placed into the darkened second stage of a two-stage chemostat, the Chlorella colonies rapidly washed out of the culture, leaving only the unicellular Chlorella supplied from the primary chemostat.

Colony growth was a `budding' process, based on visual observations. Individual cells of the colony grew in size while dividing into daughter cells; the new colony then separated from the original colony by tearing or breaking the original mother cell wall. We have replicated this experiment many times, and have observed the formation of Chlorella multicells in about 70% of the replicates.

So, the Chlorella cells in this experiment transitioned from being unicellular to multicellular whilst subject to the relevant predation pressure. During the initial transitional phase, colonies of disparate sizes were observed, but colonies containing large aggregates of cells eventually disappeared, and the steady-state achieved at the end of the experiment consisted of 8-cell colonies. This 8-cell conformation allows each cell to have a maximum surface area available for the absorption of nutrients to power photosynthesis, but renders the colony too large for the predator to consume by its usual means. Larger cell conformations are even more resilient to predation, but have lower per-cell surface area available for nutrient absorption. Which means that the conformation was driven by two selection pressures, one defined by predation, one defined by the trophic requirements of the Chlorella cells, and eventually, the culture stabilised upon a conformation that optimised the performance of those colonies with respect to the two selection pressures.

Moving on:

,blockquote>Observations of predation events

In our video microscopy observations of predation events between Ochromonas and Chlorella, unicells and `neonatal' colonies were eaten. Although the typical feeding behaviours were expressed on unicells and small colonies (Boraas et al., 1992), the O. vallescia failed to ingest fully grown colonies larger than about 15 μm. The smaller of the young or `neonatal' colonies (10-12 μm), about the size of the eight-celled `buds' in Fig. 1a, could be ingested. Flagellates with food vacuoles containing a single `neonatal' colony were seen on occasion, but this vulnerable size class was rare in the cultures. The `young' colonies rapidly grew to full size by increasing individual cell volumes.

Oh look. Another response to the predation selection pressure - rapid growth of cells to ensure that the colony became immune to predation. Nice.


Our experiments demonstrate the power of predation as a single selective force in promoting increased morphological complexity, within a short time frame. In a system where environmental conditions were held constant, a multicellular organic form evolved from a unicellular one within 10-20 generations. Based on our data and observations, the multicellular Chlorella, a rare genetic mutant in unicellular culture, was selected over unicells by Ochromonas predation. In the presence of phagotrophs, there was a clear selection mechanism for colony formation: unicells and colonies with small, young cells could be eaten, whereas colonies with larger cells could not. Since Chlorella is obligately asexual, sexual recombination does not cloud the issue.

Mechanisms for formation of multicellular Chlorella and regulation of colony size

During normal unicellular cell division and growth, Chlorella divide into 2-16 daughter cells, followed by a split of the mother cell wall and subsequent dispersal of the neonatal cells; empty mother cell walls are interspersed with whole cells at a ratio of about 1:4. That is, about 75% of Chlorella divisions are into two daughter cells and 25% into four daughter cells (Fott and Novakova, 1969; Williams, 1971). We have repeatedly observed the same pattern in our Chlorella continuous cultures since 1974 (Boraas, 1979).

In continuous cultures with the predator, the rapid appearance of very large multicellular Chlorella (Fig. 1c) apparently resulted from incomplete division: an initial loss of the mechanism for separating successive generations. The most probable initial mechanism for colony formation, adhesion of the daughter cells to the mother cell wall, is suggested by two observations: the membrane that surrounds the colonies (Fig. 1d) and the absence of cast-off mother cell walls in cultures dominated by colonial morphs (personal observation). Incomplete cell division has also been proposed as a mechanism for selection of elongated bacteria in the presence of protozoan predation (Shikano et al., 1990; Gillott et al., 1993).

Two potential mechanisms for reducing colony size were suggested from electron micrographs of multicellular Chlorella. First, the original mother cell wall became increasingly fragile in multicells. The enclosing membrane of colonies from cultures 20-100 days old had a `ropy' appearance (Fig. 1a). Such `ropes' could form if the mother cell wall split and curled on itself, unlike wild-type cell walls. As the daughter cells grew, the `ropy' form may have broken more readily than the earlier `sheet' form of the mother cell wall (Fig. 1d). Secondly, colonial cells shared cell walls (Fig. 1f: two cells, from a culture 540 days old). One of the cells (Fig. 1f) was dividing, implying division may not have been synchronous within colonies. As the cells grew and their radii increased, the cell walls would slowly tear apart, with separation occurring at some critical radius.

So, we have detailed observations of the appearance of a multicellular organism from one that was previously unicellular. Moreover, those observations include detailed analysis of the physical mechanisms by which the organisms can become multicellular.

Moving on:

Alternative hypotheses

Our results could be interpreted as evidence that the flagellates released a substance inducing colony formation in Chlorella, similar to predator-induced morphological changes in zooplankton (Dodson, 1989) and in coccoid green algae (Hesssen and van Donk, 1993). We discount this alternative hypothesis, based on four observations. First, colonies did not become apparent for about 20 Chlorella generations after inoculation of the flagellates. An `induction' should have been expressed as soon as the inducing substance produced by the flagellates had reached some critical concentration. Secondly, once it has appeared, the colonial growth form has been maintained in mixed-species cultures for over 2 years, even at low flagellate densities. Induction should vary with flagellate density. Thirdly, when the colonies are cultured in the absence of any source of an inducing substance, the colonies `breed true'. The colonial Chlorella morph remains colonial both on agar and in monospecific liquid culture, including chemostats where steady states have been maintained for several months. Finally, in nitrogen-limited, two-stage chemostats where both stages are illuminated, with unispecific Chlorella in the first stage and mixed Chlorella-Ochromonas in the second stage, we see colonial Chlorella. These Chlorella must be growing on the inorganic nitrogen excreted by Ochromonas. When the second stage is darkened, the Chlorella colonies rapidly wash out of the culture, leaving only the unicellular Chlorella supplied from the first stage and, of course, their flagellate predators. This shows that active photosynthesis by the algae and continued interaction with the predator are essential to maintain the colonial algae in continuous culture. When cultured in the absence of the predator, the cell size of the unicells in the second stage declines, showing that cell division and associated morphogenetic processes are taking place, but the colonies are not formed in the absence of the predator.

So, the authors tested to see if an alternative hypothesis accounted for the observed results, and determined four reasons why that alternative hypothesis was not supported. Once again, real scientists doing what they do best - learn about reality.

The conclusions are lengthy, and so I shall concentrate on the important parts. Since I've already provided a link to the full paper, the full conclusions are readily readable by anyone taking the trouble to download the paper. Here's the important parts:

Significance of this experimental study to evolutionary hypotheses

Our data demonstrate that predation, as a single selective factor, can select for multicellularity in a prey organism. The Chlorella had maintained the normal unicellular body shape for thousands of generations in the same laboratory culture conditions. After about 10-20 generations in the presence of the phagotroph, an eight-celled Chlorella `colony' became the dominant phototroph in all replicates of this experiment. The data support Stanley's (1973) hypothesis for the origin of multicellular organisms: the emergence of phagotrophic unicells in the Precambrian could have rapidly selected for colonical prey, eventually resulting in the Metaphyta and Metazoa.

After a long Precambrian history of slow, unicellular evolution, multicellular life forms abruptly appeared in the late Precambrian. Stanley (1973) proposed that the `invention' of unicellular predation was the cause of the origin of multicellular phototrophs or chemotrophs in the late Precambrian. The appearance of phagotrophs or predators probably first increased potential species diversity by recycling resources (Tilman, 1982) such as space (Paine, 1966) or chemical elements (Seale, 1980). Then prey with increased body size would have a selective advantage, since such organisms could escape predation. The combination of the two processes could have contributed to the observed increase in species and structural diversity (Stanley, 1973).

Stanley's (1973) argument hinges on the observation that small-celled organisms usually have a competitive advantage for limiting mineral nutrients. In experiments where the unicells and colonies were placed in competition in the absence of the phagotroph in the light, the multicellular form was slowly displaced by unicells (data not shown). Hence, without the predator, unicells are superior competitors in our continuous culture system.

There are many examples in the literature describing adaptive trade-offs in related groups or species (Townsend and Calow, 1981; Stephens and Krebs, 1986; Bennett and Boraas, 1989; Bennett et al., 1993). The eight-celled, stable colony in our system probably expresses an adaptive `trade-off' between the two main selective pressures in our experimental system: (1) predation selected for more cells per colony, minimizing death by phagotrophy, and (2) competition for nutrients selected for fewer cells per colony, maximizing nutrient uptake per cell. In the absence of predation, Chlorella maintain a unicellular state, despite occasional mutational `mistakes'. With predation, these `mistakes' allow survival in the face of almost certain death. The single cells in the new `colony' may be at a disadvantage in a straightforward `scramble' for inorganic nutrients. However, small differences in the ability to take up nutrients would be more than offset by the large selective advantage in the ability to avoid immediate death from predation. One way to avoid such mortality is to be too large to be eaten, and hence live to reproduce rather than serve as a food source for the new predator. As long as no larger, more voracious predators enter the system (through evolution or immigration), the multicellular form can proliferate, even if at a probable competitive disadvantage.

Well look at that ... I anticipated the last paragraph reproduced above. But then that's what comes when one pays attention in biology classes.

Continuing the important part of the conclusions:

The `invention' of predation in the Precambrian itself may have led to the evolution of eukaryotic cells from prokaryotes by a process of ingestion and symbiosis (Margulis, 1981). This hypothesis is supported by extensive evaluation of contemporary genomes and other characteristics of plastids (Gray and Doolittle, 1982). Apparently, the development of a cell nucleus was a necessary prerequisite for the first predators. There are no known true phagotrophic prokaryotes, either extant or in the fossil record (Margulis, 1981). Consequently, prokaryote communities without phagotrophic nutrition (but possibly with osmotrophic parasitism) would be structured by competitive interactions, particularly differential uptake of soluble nutrients. As discussed above, osmotrophic organisms with a large surface-to-volume ratio (i.e. small cell size) can often grow more rapidly than larger competitors. The argument can be extended to communities without phagotrophs with eukaryotes and symbionts. Thus, in the absence of phagotrophy, natural selection should favour small, free-living cells, which have the greatest access to nutrients and the most effcient mechanisms for their uptake and conversion. The appearance of phagotrophy would reverse this advantage, favouring larger prey.

I'll skip the rest of your Gish Gallop in the interests of brevity.

If evolutionary scientists have no convincing answers to all these questions

They have answers for questions you were incapable of even fantasising about.

I suspect this will suffice for the time being ...

toto974's picture
A truly massive argument from

A truly massive argument from ignorance, doubled bay an argument from incredulity then the bible is true... truly astounding and worthy of an intelligent and meaningful conversation.

Simon Moon's picture
Looks like the OP might be a

Looks like the OP might be a drive by pigeon chess player.

He knocked the pieces over, crapped on the board, and flew back to its flock to claim victory.

Sheldon's picture
"Sorrentino "Evolution is a

"Sorrentino "Evolution is a scam"

...and you thought you would tell atheists on atheist forum beeecaaaause?

Let's try this, how many scientific facts apart from evolution that in no way contradict your superstitious religious beliefs do you deny?

Busted......creatards make the worst trolls.

Sorrentino "if you're not satisfy with this answer and you still insist that evolution is true and creation is false, then invite any evolutionary scientists to answer all the questions cited above (especially question 10 and 11)."

Science has evidenced species evolution through natural selection beyond any reasonable or rational doubt, all the evidence globally from over 160 years of rigorous scientific scrutiny supports it, if you have a problem with this take it up with science, instead of having a tantrum with atheists on the internet. Creationism is not supported by any objective evidence, and this will remain a fact independently of the fact of evolution, what you have produced is a known logical fallacy called a false dichotomy, or false equivalence.

Sheldon's picture
So this was another drive by

So this was another drive by theist troll, quelle surprise.

Nothing on any news network that evolution has been falsified?

Shouldn't Breezy have published his paper by now?

I believe the correct phrase is represented as PMLMAO...

Breezy was funny mind, for a creatard I mean, you have to give him that, albeit unintentionally.

Calilasseia's picture
Meanwhile, a recent

Meanwhile, a recent development published in Science is interesting with respect to this thread ... namely, the discovery that if you put the eggs of Xenopus laevis frogs in an ultrasound blender, so that the cells are completely disrupted, and then leave the resulting emulsion standing, the emulsion re-organises itself into recognisable cells, which then continue dividing once they've re-formed.

Furthermore, this process can take place in the presence of chemicals that inhibit several of the known regenerative processes previously found to be in operation in Xenopus egg cells.

Cognostic's picture
Cali: How is it you find

Cali: How is it you find time to spend on a simple atheist site? Your lucidity is unparalleled and your compendious style, always a pleasure to read. I imagine individuals with such eloquence to be frequenting the halls of their very own atheist pages, traveling, lecturing, writing books or otherwise engaged in the betterment of mankind on this little blue ball. You make me feel like I should have paid more attention in English class.

algebe's picture
If evolution is a scam, that

If evolution is a scam, that crime has involved every university with a biology department for over 100 years. Who's coordinating this vast conspiracy, and for whose benefit? I just can't any way to profit from this so-called scam.

On the other hand, a lot of money has changed hands as a result of creationist nonsense, most notably that monstrous boat in Kentucky. If you want to find a scam, follow the money.

Sheldon's picture
Algebe "Who's coordinating

Algebe "Who's coordinating this vast conspiracy, and for whose benefit? "

Precisely, cue another unevidenced theist assertion for an invisible nefarious demon called Satan.

Vex_Man's picture
> (2) What later caused some

> (2) What later caused some of these self-replicating cells to abandon their diploid way of life and suddenly change to become haploid cells (meiotic cell division)—an event that make sexual reproduction to be possible— ?

Since we have no fossilized vestiges that is remained of the very first replicator, we have some good speculations only. But that does not mean scientists cannot recreate DNA in future for demonstrating --'how life has arisen'. If we do not know anything, that does not mean 'your God did it'. You can put million number of conceivable things instead of God. Thus, the probability of God's existence is barely 0.000001. (as 1/million= 0.000001)

> ( 3) What later caused two of these haploid cells to start fusing with one another during sexual reproduction in order to restore their original diploid state ( fertilization) ?

Meiosis is the process that divides cells and reduces chromosomes' numbers (in parent cells) to 1/2. The chromosomes restored when egg and sperm combine and create a single cell.

> (4) What later caused this fused cell (called zygote) to multiply and form a compact ball of similar cells (mitotic cell division) ?

> (5) What later caused this compact ball of similar cells to "differentiate" and "specalize" to form different types of cell (like bone cells, muscle cells, blood cells, nerve cells, skin cells, cartilage cells, epithelial cells, endothelia cells, liver cells, kidney cells, brain cells, retinal cells etc) using a complex cascade of genetic program known as developmental gene regulatory network (dGRN) ( cellular differentiation) ?

Both were caused by 'cell fusion'. Cell fusion is a process that is known for combining many single nucleus cells into a multi-nuclear cell.

> (6) What if the similar ball of cells just continue to multiply (like what we observed with cancer cells ) and never stop to start differentiation process ?

If similar ball of cells continue to multiply and never quit to initialize differentiation process, then cells will not be able to manage their functions properly.

> (7) Besides, how did last ball of cell to multiply get to "know" that it is time to stop multiplication and start the differentiation process ?

It got to know thru embryogenesis. Embryogenesis is a process which helps to form and to develop embryo.

I cannot answer your all questions because I do not have 'that much time'. If I recall anything relevant to your questions' answer, I will edit this post.

Grinseed's picture


In his book for the educated layman,"Endless Forms Most Beautiful" Sean B. Carroll tells the history of how we now understand how genes "know" when to start and stop specific protein and cell production and how mutations occur during the lifetime of any single organism. It is based on ongoing research from the 1950s after the double helix structure was understood which eventually revealed the existence of homeoboxes, or toolkits, as geneticists like to call them, with specific gene sequences that act like blueprints for how the genes determine the size shape and details of a developing organism through its lifetime.

The most surprising revelation of all is that every organism alive shares the same homeobox in their genes. From the bacteria Esherichia coli to elephants to humans, the homeotic toolkit shares the same features and operations in genetic management. This further supports the interrelated nature of all life and its shared origin. It is a must read for anyone like you Sorrentino to read and understand in honest pursuit of the workings and understanding of life.

OK great book. One thing it, or evolutionary research does not do, is disprove the existence of gods or the supernatural. That is not the purpose of science nor evolutionary research. (It is "E=mc 2" not "E=mc 2, there fore god does not exist".) Science is a strict self-correcting methodology (if a scientist is wrong, he will be told in no uncertain terms - scientists are empahtically strict on evidential proof). It does not claim understanding of all things and even holds what it has made understandable may yet prove incorrect or incomplete with new research and evidence.

However what evolutionary research has also not determined is that there is any singular godly guiding purpose behind the fact of life. Everything in modern evolutionary science is supported by the natural interactions of physics and chemistry. Nothing else is needed to explain how things operate. If the scientific explanation is not enough for the spiritually minded then by all means they can claim their god created everything with out explanation, including evolutuonary theory.
I have always thought that if there were an omnipotent god worthy of worship, evolution would be a far more appropriate display of divine power, than just making things appear, seemingly out of nothing, like some Vegas magician.

Its an impossible and pointless protest to discard evolutionary science. Evolution is a fact. Its not just part of the curriculum of biology, it IS biology. It is now the basis of our whole medical knowledge. What will you replace it with? Prayer and thoughts? We've already been there and it pointedly did not work. The standout issue of modern medicine is that viruses and bacteria EVOLVE and without the evolutionary research at the heart of modern medicine we would not have been able to deal with any of the viral epidemics or diseases that have afflicted mankind for the past 100 years. We all need to attempt to understand these processes that scientists have been unravelling to protect ourselves and to help us understand just how majestic this natural world is.

Perhaps you might channel some of the energy of your faith towards promoting better understanding and knowledge of this reality you believe is created, rather than seek to destroy it because it doesn't fit the stories of your single holy book, which has never been intended to be taken literally, only liturgically.

edited for errors caused because I can't control time

Cognostic's picture
RE: Evolution is a scam.

RE: Evolution is a scam.
Sorry I am late to the party. Evolution is a scam? Ha ha ha ha - give me a break. I just came from the annual Evolution Is Not a Scam Conference and Retreat in Lake Arrowhead California. Unless you change and evolve beyond little children you'll thwart the evolutionary process and your children and your children's children will revert to their apelike ways. If you do not repent you will be cast into the gene pool of ignorance and lost forever.

The wages of ignorance is de-evolution. If you do not turn from your faith you will de-evolve. You will become as apes. It's that simple, you either turn or you begin eating bananas.

Evolution so affected the world that it gave its only begotten species of apelike creatures the ability to generate self awareness and become the human species we know today. But humans in their ignorance sin against evolution and risk de-evolution. The path to the future is narrow and not all of us are going to make it. Embrace evolution as the truth today and save yourself and generations to come from becoming the feral beasts of the forest they once were. Assuming evolution to be non-scientific is just ignorance. Equating it with a region, doubly so. Believe now or risk becoming your ape like nature and destroying the lives of your own future generations.

And NOW, for a limited time only, you can get your very own, gold embossed, book of Darwin. Just reading this book will prove that your mind is developed enough to evolve. Be the first on your block to evolve to the next level. Be popular with your friends. All this can be yours for just $29.95. Hurry now why supplies last. Show everyone what an evolved creature you have become!

ilovechloe's picture
@Sorrentino -

@Sorrentino -
Even if I believed that everything that you wrote is true & factual (I don't), it still doesn't prove 'creation' & a god did it.

You are relying on the fact that the average lay person will not have enough scientific knowledge in this area to know what you are talking about, & hopefully be dazzled by all the 'scientific sounding' terminology & jargon you are writing. I suspect that you also have no real idea what it all means, & are merely cutting & pasting from a creationist website.

Even if you could somehow prove that a 'god' did it, then you would still need to prove that the particular god that you believe in did it!

So even if you could prove that evolution is false (do so & you will no doubt become famous & make lots of money), you are still no closer to proving that whatever particular brand of religion that you believe in is also valid, out of the thousands of other religions that exist or existed!

Instead of wasting time on an atheist forum, why don't you do some proper research into your so-called 'theory of creation' & publish some papers in some credible scientific journals to have them peer-reviewed (when I say credible scientific journals, I am not talking about the creationist 'scientific' journals that have been setup by creationists to try to make creationists look more credible).

Maybe then we can start to take you more seriously!

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