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Re: OP (Before reading any other responses.)
Hey there, Stephen! Welcome to the AR. If you are sincerely interested in legitimate discussions as you state, then nice of you to join us. Otherwise, you are going to be in for a bumpy ride... *chuckle*... For the moment, at least, I admit I am interested in hearing what you have to say. Speaking of which, there was a part of your OP that caught my attention, and I would be interested in a little more insight from you if you don't mind. For starters, you claim you were once a "hard core nihilist atheist." Then, you went on to state...
"I converted to christianity in late 2011 after a series of near death incidents in Afghanistan (no, not the "I went to heaven and saw Jesus" type stuff, just "whoa I almost died back there" type stuff, and no I wasn't in the military)"
Basically, I am just rather curious as to what it was about those "near death incidents" that caused you to seek out Christianity to praise and worship the god that (by your own beliefs) put you in those situations in the first place. Not to mention the same god that is responsible for the horrendous living conditions most of the people in that country are forced to endure. Personally, those are things that make me LESS likely to want to turn to that particular god. But, wait. My apologies. I am getting ahead of myself. Allow me to tell you a bit about me real quick. (Readers' Digest condensed version...)
* Raised as a Christian (Baptist/Methodist) in a small town in the Bible Belt
* Was finally able to fully escape my religious indoctrination and consider myself an atheist within the last couple of years
* Was military (Army National Guard) and deployed to Afghanistan once and to Iraq twice
* Retired from law enforcement in a large crime-infested city after twenty years on patrol within the worst neighborhoods in that city
* Lost many good friends along the way, with the military and the police department
* Along the way, I was involved in more "near death incidents" that I can possibly remember. Some of those incidents were just "non-personal" events (wrong place at the wrong time, accidents, natural causes, etc.). Some of those incidents were other people intentionally trying to kill me. (Keep in mind, however, these are just the work/military related incidents. I can't even begin to recall all the times I probably should have died due to my own stupidity doing some of the outlandish shit I considered to be fun, even when I was just a little kid... *chuckle*...)
Anyway, with that bit of "history" in mind, I do not recall a single time during any of those countless moments that I EVER felt the need to run back to my church, fall to my knees, and thank god for "saving my life." Honestly, the thought never occurred to me, not even during some of my "stronger belief" days. Moreover, I have never experienced any type of PTSD that today seems to be so dreadfully common with folks who have experienced "traumatic situations." I would be involved in a violent situation. I would maybe get roughed up a bit and/or possibly nearly killed. When it was over, I would pick myself up (if I was able), dust myself off, go get stitches and/or other medical attention (if necessary), and go back to business as usual. Simply was not a big deal to me.
Now, I have worked with many brave men and women who have experienced many of the same things I have. (And some worse things.) For the most part (best that I was able to tell), many of them handled it all rather well. However, I have seen others that have totally "lost their shit" and damn-near became "basket cases" after experiencing incidents I would have rated not worthy of so much as a raised eyebrow. And that is why I ask you about why your "close calls with death" somehow pushed you toward religion, because I honestly and sincerely cannot relate to that type of mindset. I am curious about your thoughts on that.
(Okay, now to go see what everybody else is saying...)
Well, damn... *hands on hips*... Just finished reading all the other responses, and it looks like I will never get my answer from Stephen. As usual, you bunch of godless heathens with your annoying logic and reason have done gone and sent another theist running away with his tail tucked between his legs.... *throwing hands up in exasperation*... I SWEAR, I can't take you people ANYWHERE!... *storming away toward break room*... COG! Get your grubby little monkey hands off of my whiskey bottle!
What objective evidence can you demonstrate for any deity?
Oh dear, someone has erected canards about eye evolution. Oh dear. And appears to be unaware that there's a wealth of scientific literature covering the evolution of morphological change on time scales a lot shorter than several million years. I'll now cover some appoiste examples of both.
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 , and the abstract reads thus:
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:
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:
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:
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?
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:
 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;
 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;
 The epigean phenotype fishes have arisen from hypogean ancestors.
 is considered unlikely by the authors, given the known geography of the cave system, but is required to be ruled out evidentially.  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. , 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:
Now, comes the analytical results!
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.
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:
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:
 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;
 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.
In other words, more severe eye defects;
 Ectopia pupillae - failure of the pupil to be properly centred;
 Foveal hypoplasia - failure of the fovea to develop fully during embryogenesis, inheritance again autosomal dominant;
 Autosomal dominant keratitis - opacity of the cornea with accompanying vascularisation, often associated with foveal hypoplasia above;
 Ocular coloboma - abnormal development of the optic cup and stalk, accompanied by holes appearing in various eye structures;
 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:
ATGCAGAACA GTCACAGCGG AGTGAATCAG CTCGGTGGTG TCTTTGTCAA CGGGCGGCCA 60
CTGCCGGACT CCACCCGGCA GAAGATTGTA GAGCTAGCTC ACAGCGGGGC CCGGCCGTGC 120
GACATTTCCC GAATTCTGCA GGTGTCCAAC GGATGTGTGA GTAAAATTCT GGGCAGGTAT 180
TACGAGACTG GCTCCATCAG ACCCAGGGCA ATCGGTGGTA GTAAACCGAG AGTAGCGACT 240
CCAGAAGTTG TAAGCAAAAT AGCCCAGTAT AAGCGGGAGT GCCCGTCCAT CTTTGCTTGG 300
GAAATCCGAG ACAGATTACT GTCCGAGGGG GTCTGTACCA ACGATAACAT ACCAAGCGTG 360
TCATCAATAA ACAGAGTTCT TCGCAACCTG GCTAGCGAAA AGCAACAGAT GGGCGCAGAC 420
GGCATGTATG ATAAACTAAG GATGTTGAAC GGGCAGACCG GAAGCTGGGG CACCCGCCCT 480
GGTTGGTATC CGGGGACTTC GGTGCCAGGG CAACCTACGC AAGATGGCTG CCAGCAACAG 540
GAAGGAGGGG GAGAGAATAC CAACTCCATC AGTTCCAACG GAGAAGATTC AGATGAGGCT 600
CAAATGCGAC TTCAGCTGAA GCGGAAGCTG CAAAGAAATA GAACATCCTT TACCCAAGAG 660
CAAATTGAGG CCCTGGAGAA AGAGTTTGAG AGAACCCATT ATCCAGATGT GTTTGCCCGA 720
GAAAGACTAG CAGCCAAAAT AGATCTACCT GAAGCAAGAA TACAGGTATG GTTTTCTAAT 780
CGAAGGGCCA AATGGAGAAG AGAAGAAAAA CTGAGGAATC AGAGAAGACA GGCCAGCAAC 840
ACACCTAGTC ATATTCCTAT CAGCAGTAGT TTCAGCACCA GTGTCTACCA ACCAATTCCA 900
CAACCCACCA CACCGGTTTC CTCCTTCACA TCTGGCTCCA TGTTGGGCCT AACAGACACA 960
GCCCTCACAA ACACCTACAG CGCTCTGCCG CCTATGCCCA GCTTCACCAT GGCAAATAAC 1020
CTGCCTATGC AACCCCCAGT CCCCAGCCAG ACCTCCTCAT ACTCCTGCAT GCTGCCCACC 1080
AGCCCTTCGG TGAATGGGCG GAGTTATGAT ACCTACACCC CCCCACATAT GCAGACACAC 1140
ATGAACAGTC AGCCAATGGG CACCTCGGGC ACCACTTCAA CAGGACTCAT TTCCCCTGGT 1200
GTGTCAGTTC CAGTTCAAGT TCCCGGAAGT GAACCTGATA TGTCTCAATA CTGGCCAAGA 1260
Here's the protein it codes for, again nicely formatted using my applet:
(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:
TATCGATAAG TTTTTTTTTT ATTGTCAATC TCTGTCTCCT TCCCAGGAAT CTGAGGATTG 60
CTCTTACACA CCAACCCAGC AACATCCGTG GAGAAAACTC TCACCAGCAA CTCCTTTAAA 120
ACACCGTCAT TTCAAACCAT TGTGGTCTTC AAGCAACAAC AGCAGCACAA AAAACCCCAA 180
CCAAACAAAA CTCTTGACAG AAGCTGTGAC AACCAGAAAG GATGCCTCAT AAAGGGGGAA 240
GACTTTAACT AGGGGCGCGC AGATGTGTGA GGCCTTTTAT TGTGAGAGTG GACAGACATC 300
CGAGATTTCA GAGCCCCATA TTCGAGCCCC GTGGAATCCC GCGGCCCCCA GCCAGAGCCA 360
GCATGCAGAA CAGTCACAGC GGAGTGAATC AGCTCGGTGG TGTCTTTGTC AACGGGCGGC 420
CACTGCCGGA CTCCACCCGG CAGAAGATTG TAGAGCTAGC TCACAGCGGG GCCCGGCCGT 480
GCGACATTTC CCGAATTCTG CAGGTGTCCA ACGGATGTGT GAGTAAAATT CTGGGCAGGT 540
ATTACGAGAC TGGCTCCATC AGACCCAGGG CAATCGGTGG TAGTAAACCG AGAGTAGCGA 600
CTCCAGAAGT TGTAAGCAAA ATAGCCCAGT ATAAGCGGGA GTGCCCGTCC ATCTTTGCTT 660
GGGAAATCCG AGACAGATTA CTGTCCGAGG GGGTCTGTAC CAACGATAAC ATACCAAGCG 720
TGTCATCAAT AAACAGAGTT CTTCGCAACC TGGCTAGCGA AAAGCAACAG ATGGGCGCAG 780
ACGGCATGTA TGATAAACTA AGGATGTTGA ACGGGCAGAC CGGAAGCTGG GGCACCCGCC 840
CTGGTTGGTA TCCGGGGACT TCGGTGCCAG GGCAACCTAC GCAAGATGGC TGCCAGCAAC 900
AGGAAGGAGG GGGAGAGAAT ACCAACTCCA TCAGTTCCAA CGGAGAAGAT TCAGATGAGG 960
CTCAAATGCG ACTTCAGCTG AAGCGGAAGC TGCAAAGAAA TAGAACATCC TTTACCCAAG 1020
AGCAAATTGA GGCCCTGGAG AAAGAGTTTG AGAGAACCCA TTATCCAGAT GTGTTTGCCC 1080
GAGAAAGACT AGCAGCCAAA ATAGATCTAC CTGAAGCAAG AATACAGGTA TGGTTTTCTA 1140
ATCGAAGGGC CAAATGGAGA AGAGAAGAAA AACTGAGGAA TCAGAGAAGA CAGGCCAGCA 1200
ACACACCTAG TCATATTCCT ATCAGCAGTA GTTTCAGCAC CAGTGTCTAC CAACCAATTC 1260
CACAACCCAC CACACCGGTT TCCTCCTTCA CATCTGGCTC CATGTTGGGC CTAACAGACA 1320
CAGCCCTCAC AAACACCTAC AGCGCTCTGC CGCCTATGCC CAGCTTCACC ATGGCAAATA 1380
ACCTGCCTAT GCAACCCCCA GTCCCCAGCC AGACCTCCTC ATACTCCTGC ATGCTGCCCA 1440
CCAGCCCTTC GGTGAATGGG CGGAGTTATG ATACCTACAC CCCCCCACAT ATGCAGACAC 1500
ACATGAACAG TCAGCCAATG GGCACCTCGG GCACCACTTC AACAGGACTC ATTTCCCCTG 1560
GTGTGTCAGT TCCAGTTCAA GTTCCCGGAA GTGAACCTGA TATGTCTCAA TACTGGCCAA 1620
GATTACAGTA AAAAAAAAAA AAA 1643
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 ...
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:
 Substitution of codon triplet for W (tryptophan) replacing G (glycine) at codon position 18 (bp 52-54);
 Subsititution of codon triplet for R (arginine) replacing G (glycine) at codon position 26 (bp 76-78);
 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;
 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?
Oh dear. The hard evidence from the real world supports evolution. Let's look at the next paper:
Oh look. More hard evidence from the real world supporting eye evolution. Namely that:
 Different cave fish populations evolved the eye apoptosis mechanism independently, and have different mutations coding for this;
 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;
 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;
 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.
However, the best part is when we look at the article in detail ...
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 whole brace of animal phyla from flatworms to mammals, including you and I.
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):
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.
Meanwhile, there are other instances of morphological change driven by evolutionary processes, that occur in relatively short time frames. One apposite and classic example is this paper on Croatian lizards:
Rapid Large-Scale Evolutionary Divergence In Morphology And Performance Associated With Exploitation Of A Different Dietary Resource by Anthony Herrel, Katleen Huyghe, Bieke Vanhooydonck, Thierry Backeljau, Karin Breugelmans, Irena Grbac, Raoul Van Damme, and Duncan J. Irschick, Proceedings of the National Academy of Sciences of the USA, 105(12): 4792-4795 (25th March 2008) [Full paper available in HTML format on the PNAS website here, also available as a PDF download from the same website via this link]
Now, at this point everyone will probably be reeling from the sheer mass of material, but the point I'm hammering home with this little lot is that we have a vast body of evidence from PRESENT DAY LIVING ORGANISMS supporting evolutionary postulates, which means that even if there were no fossil record to call upon, the empirical evidence obtained by geneticists and other biologists would be more than sufficient to support evolutionary theory. Fossils provide us with some nice instances of icing on the evidential cake (e.g., Tiktaalik and Archaeopteryx), but the most subtantial body of hard evidence for evolution these days comes from living organisms, and the ever-growing mass of results from genetics laboratories.
Let's examine this paper in more detail, shall we?
First of all, here's the abstract:
So even in the abstract, the authors specifically state that they consider the changes involved to have been the product of evolutionary forces.
Moving on, we find this on page 4793 of the paper:
So, the authors explicitly state that the trophic migration to a new dietary resource provided a selection pressure driving the development of features facilitating more efficient exploitation of that resource over the course of 30 generations. Easily observable within the lifetime of relevant human researchers, as demonstrated in this paper.
Moreover, phenotypic plasticity is understood by real biologists to be yet another source of variation upon which evolutionary forces and selection pressures can act. In this case, migration into a new trophic niche, involving the introduction of fibrous plant matter into the diet by the transplanted Pod Mrcaru individuals, provided the selection pressure required to drive the development of relevant new features. Once the lizards changed their diet, and began integrating fibrous plant matter into that diet, there existed a selection pressure favouring any individuals inheriting mutations resulting in more efficient occupancy of that new niche. Consequently, any individuals that developed the requisite mutations would disseminate those mutations to their offspring, and those offspring would be able to perform more efficiently in that niche, which means that they would have a selective advantage over other lizards not possessing those mutations. Plus, since it has been demonstrated that phenotypic plasticity arises from a genetic origin in numerous organisms (for example, I have a paper on diphenic caste development in honeybees, which is intimately coupled to the TOR gene), those genes are manifestly subject to selection pressures.
So, according to this paper, the changes took just 30 generations to complete, which means that these lizards apparently evolved the changes to their morphology at an extremely fast rate. It is possible that this is the result of gene-based phenotypic plasticity of course, in other words, the lizards possessed the genes required to respond to environmental changes prior to their transplantation, and that said transplantation introduced a strong positive selection for the development of that plasticity in the observed direction. An analogous situation arises among Cichlid fishes, which possess considerable phenotypic plasticity with respect to their feeding apparatus (most notably the pharyngeal jaw mechanism) which allows these fishes to radiate into new trophic niches rapidly, a factor that contributed to the rapid speciation events recorded with respect to the Lake Victoria Superflock. This is a grouping of fishes with a known common ancestor (they are derived from an ancestral population of Haplochromis gracilior from nearby Lake Kivu), as determined by the requisite molecular phylogenetic analysis (the paper in question being Origin of the Superflock of Cichlid Fishes from Lake Victoria, East Africa by Erik Verheyen, Walter Salzburger, Jos Snoeks and Axel Meyer, Science, 300: 325-329, 11 April 2003), but which has radiated in just 12,400 years into 350+ species that have been described by science. Sexual selection and trophic specialisation upon discovering new niches are considered to be the driving factors behind the rapid speciation of these fishes, and Cichlid fishes have been known to possess considerable pharyngeal and dental phenotypic plasticity since Dr Humphrey Greenwood's landmark paper on the subject in 1977.
Once again, this is something that is easily understood by those of us who pay attention to REALITY instead of mythological horseshit.
Indeed, the appearance of both increase bite force allowing better consumption of the new dietary resource, and the appearance of caecal valves in the intestine facilitating superior utilisation of the new dietary resource at the digestion stage, were both selected for. If they hadn't been selected for, they would not have appeared.
This isn't the only example of rapid morphological change driven by evolution that I could present here, with other examples such as the ectodysplasin-mediated development of armour plates in sticklebacks and the Double Tail mutation in Betta splendens being but two examples I could cover in detail, but this post would start to turn into an encyclopaedia in its own right if I provided full expositions thereof in this post, and might even crash the server. That's before we cover such data as that presented in the landmark Lenski paper on Escherischia coli, and the hilarity surrounding Lenski's napalming of Andrew Schlafly's canards on the subject.
Oh, and as for our being unable to reproduce another Big Bang, the moment when we are able to do so could come a lot quicker than you think. for more on this, read this previous post of mine, covering the work of Steinhardt & Turok, two leading cosmological physicists. I might address planetary accretion at some later date if I can find relevant papers.
Thanks again for your erudite and entertaining posts...copied for later digestion and definite regurgitation (with credit of course)
LOL....some theists just don't know what will hit them....ahahahahahha!
@ Calli: Thank you Brother Cali: I had not the time, inclination, attention span or energy to attack than inane wall of text. Nice to have you around.,
@StephenStoned: I have three confirmed atheist kills.
You know I find that very hard to believe from someone who turns tail and runs back under his creationist rock at the first sign of reasoned argument.
Unless he wanders under bridges with a few bottles of wine and gets some poor soul to listen and agree for a taste of alcoholic forgetfulness.
@Algebe Re: Stephen's "three confirmed atheist kills"
Yeah, like you, I find his claim considerably farfetched. The way he bailed out of here so quickly after just a few questions on a website where we are all "anonymous" makes it incredibly difficult for me to believe he has the backbone to stand face-to-face with a real adult atheist who is likely making even tougher arguments.
With that in mind, notice Stephen never stated the atheists he "converted" were adults.... *raising an eyebrow*... For all we know, those "atheists" could have been children between two and three years of age. Based on what he presented during his short stay here, I'm guessing that's about the oldest age he could handle in a debate, anyway.
I bet the Taliban loved that. Though it would explain the near death experiences.
Again all I can do is reiterate, what objective evidence can you demonstrate for any deity?
@Sheldon: "Non-denominational" *Throat Clearing sounds* "Aheeemmm ---"
Hey Sheldon? Aren't we...... um...... well.......... um......... non-denominational too?"
Wouldn't being non-denominational be a move towards atheism. I pretty much think all atheists are non-denominational. When I ask myself which denomination I belong to.... I just can't think of any. How about you??? Any other atheist out there belong to a denomination?
As you say Cog., I'm unaffiliated, as are all atheists I suppose.