Oh look. I thought it wouldn't be long before our latest mythology fanboy outed himself not only as a creationist, but, like every other creationist I've ever encountered, a duplicitous creationist into the bargain. The tell tale signs were present long before he bailed out of the original thread and launched this latest one.

So, let's take a look at this latest tsunami of tard, shall we?

First, I will recap the basics of the evidence which I have already shared on this forum.

Here's a clue for you, boy. Blind assertions and ex recto apologetic fabrications do not constitute "evidence", except perhaps of your own inadequacy.

If you look at a building, what evidence do you need in order to know that there was a builder? The building is the evidence. A building does not build itself.

Oh dear, not this fatuous apologetic horseshit.

What part of "we have observational data telling us that humans build houses and other buildings" do you not understand?

First of all, no one here is doubting for a moment, that manifest human artefacts are produced by humans. But I'm used to this level of discoursive inadequacy emanating from creationists.

Similarly, if you study a painting, regardless of how you interpret the brush strokes or what you believe the artist intended to communicate through the painting, you already know that there was in fact, an artist. The painting itself evidences that. Paintings do not paint themselves; if there is a painting, surely there was a painter.

And once again, no one doubts that manifest human artefacts are the product of humans.

But please, do continue displaying your inadequacy here.

Before we get to the next part, I would like to quote Charles Darwin:

“If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find no such case.”

Refreshing to see that for once you didn't resort to the usual quote mining we see from your ilk ...

What about the heart? How can the human heart exist if it was made by successive slight modifications? If that were the case, it would not have functioned and would have been phased out.

The heart needs blood in order to exist and maintain proper function, yet the blood needs the heart to pump it. And what about the blood? It needs veins to flow through, but the veins need the blood in order to exist and maintain proper function, and they need the heart to pump the blood through them, or else they would have no purpose and would have been phased out, according to your own theory.

Bullshit.

First of all, you obviously never paid attention in a biology class, otherwise you would have learned that there are organisms that don't possess blood of the sort we possess, and for that matter, don't have a closed circulatory system. Arthropods have haemolymph, not blood, and also have an open circulatory system. For that matter, there are organisms that don't possess even haemolymph or a heart, but still manage to function - Cnidarians being the classic example.

Then of course, it's obvious that you obtained this drivel from some sad little creationist apologetics website, and drank their Kool-Aid uncritically, without bothering to ask yourself the elementary question of whether or not you were being lied to. I've never encountered a piece of creationist apologetics that didn't contain at least one egregious lie somewhere along the line, and this is no exception.

Evolution of the heart? Strap yourself in for the roller coaster ride, boy. Starting with the numerous scientific papers covering the evolution of the heart, such as:

Gene Regulatory Networks In The Development Of The Heart by Eric N. Olson, Science, 313: 1922-1927 (29th September 2006)

The heart, an ancient organ and the first to form and function during embryogenesis, evolved by the addition of new structures and functions to a primitive pump. Heart development is controlled by an evolutionarily conserved network of transcription factors that connect signaling pathways with genes for muscle growth, patterning, and contractility. During evolution, this ancestral gene network was expanded through gene duplication and co-option of additional networks. Mutations in components of the cardiac gene network cause congenital heart disease, the most common human birth defect. The consequences of such mutations reveal the logic of organogenesis and the evolutionary origins of morphological complexity.

Further on in the paper:

Evolutionary Advancements of the Heart

The most fundamental functional units of all hearts are cardiac muscle cells, which express an array of contractile proteins, such as muscle actin, myosin, troponin, and tropomyosin. The appearance of muscle cells preceded the divergence of Cnideria (hydra, jellyfish, and corals) and Ctenophora (comb jellies) from the Bilateria, from which mammals descended (~700 million years ago) (Fig. 1) (5). Primordial muscle cells probably resembled the epitheliomuscle cells of Cnideria and amphioxus, which is thought to be the closest living approximation of the invertebrate ancestor of vertebrates (6–8). These cells probably existed in a primitive gastric pocket where they participated in fluid movement during feeding. Muscle cells in bilaterians are derived from mesoderm, which is believed to have arisen from the gastrodermis of a diploblastic ancestor. The diversification of muscle cells gave rise to skeletal, cardiac, and smooth muscle cells, and further specialization of cardiac muscle cells ultimately yielded atrial and ventricular myocytes, as well as the cells of the mammalian cardiac conduction system.

Later on, the author provides this:

The heart of Drosophila, referred to as the dorsal vessel, also functions as a linear peristaltic pump but, in contrast to the hearts of tunicates and amphioxus, it ends in a closed cardiac compartment and contains a cardioaortic valve that separates a posterior lumen and an anterior aorta-like structure (Fig. 3) (1, 2). Nematodes do not possess a heart per se, but their pharynx contracts like a heart, and the muscle cells that line its walls exhibit electrical activity similar to that of mammalian cardiomyocytes (12).

During evolution, the heart evolved from a single-layered tube with peristaltic contractility to a more efficient and powerful pump with thick muscular chambers dedicated to receiving (atrial) and pumping (ventricular) blood, displaying synchronous contractions and seamless connections to a closed vascular system (10, 11). The transition from an aquatic to a terrestrial environment required several additional adaptations of the heart to separate oxygenated and deoxygenated blood (Fig. 2). The hearts of fish contain a single atrial chamber connected directly to a ventricle. Amphibians have two atria separated by a septum and a single ventricle. Terrestrial vertebrates have divided hearts in which septae separate the oxygenated and deoxygenated blood within the pulmonary and systemic circulations. Efficient unidirectional blood flow into and out of the heart was ensured by the appearance of valves. The conversion of a primitive heart tube to a multichambered heart that drives blood at high force through synchronous contractions also required a conduction system. Other advancements of the vertebrate heart include neural crest cells, which contribute to portions of the outflow tract and septum; trabeculae, which enhance oxygenation; the endothelium, which provides growth factor signals and precursor cells for formation of the cardiac valves; and the epicardium, which provides precursors for the coronary vasculature.

An Ancestral Genetic Network for Heart Development

Heart development is governed by a core set of evolutionarily conserved transcription factors (NK2, MEF2, GATA, Tbx, and Hand) that controls cardiac cell fates, the expression of genes encoding contractile proteins, and the morphogenesis of cardiac structures (Fig. 1). These transcription factors also regulate each other’s expression, serving to stabilize and reinforce the cardiac gene program (1, 13–15). Dozens of other transcription factors contribute to cardiogenesis, in many cases by serving as accessory factors for these core regulators.

TheMADS-box protein MEF2, which is conserved throughout the metazoans and exists even in yeast, is the most ancient myogenic transcription factor and presumably became irreversibly committed to the expression of muscle genes in an ancestral organism (16). As muscle cells diversified, MEF2 became a central component of muscle gene regulatory networks and is the only myogenic transcription factor known to be associated with the differentiation of all muscle cell types. In cardiac muscle cells, MEF2 cooperates with the core cardiac transcription factors to regulate contractile protein gene expression, whereas in skeletal muscle MEF2 cooperates with the MyoD family of bHLH transcription factors (16). Thus, MEF2 appears to have coopted different transcriptional partners to regulate different muscle gene programs via specific combinations of cis-regulatory sequences.

Within cardiac muscle lineages, Mef2 fell under the control of NK2-type homeodomain proteins, which became dedicated to cardiac muscle and associated endodermal structures (1, 13, 14, 17). Mef2 and an NK2 homeobox gene closely related to those involved in the cardiac development of bilaterians are expressed in myoepithelial cells within the gastrodermis of Cnidarians, which do not contain a heart (Fig. 1), suggesting that these genes were already associated with the muscle gene program in the common ancestor of these organisms (8). It has been postulated that a layer of muscle cells developing under the direction of an NK2-class gene within the endoderm of an ancestral organism, which may have been Cnidarian-like, evolved into pulsatory muscular vessels of an early bilaterian (17).

The author then provides this:

The conservation of the core cardiac transcription factors and their cardiac expression in all modern-day organisms with hearts suggest that they became coupled to the expression of muscle genes involved in contractility and pump formation in an ancestral protochordate, and such regulatory interconnections were maintained and elaborated on during the evolution of more complex cardiac structures. Gene duplications during evolution increased the number of genes encoding these core cardiac transcription factors (Fig. 1). Such duplications, coupled with the modification of cisregulatory elements, generated new patterns of gene expression; and variation in protein-coding regions conferred specialized activities, allowing the acquisition or modification of cardiac structures and functions. Consistent with the idea that new gene family members became more specialized and/or that functional redundancies masked their shared or subtle functions, mutations in cardiac regulatory genes in Drosophila, in which the cardiac regulatory network is relatively simple, often result in dramatic abnormalities in cardiac development, whereas mutations of individual paralogs of these genes in vertebrates frequently affect specific structures of the heart (such as ventricles or valves) that do not exist in the hearts of insects or more primitive organisms (1).

I'll cover some of the author's remarks on Drosophila, as these are of import later:

Gene Networks in Drosophila Heart Development

Drosophila has provided a powerful model for delineating the architecture of the cardiac regulatory network, due to the relative lack of functional redundancies in that network (Fig. 3). Formation of the dorsal vessel requires signaling by Decapentaplegic (Dpp), a member of the transforming growth factor–β superfamily; fibroblast growth factor (FGF); and wingless (Wg), which belongs to the Wnt superfamily (1). The Drosophila NK2 homeobox gene, tinman, is essential for the specification of cardiac cell fates (18, 19) and serves as a target of inductive signals for cardiogenesis (Fig. 3). Among the target genes of tinman is the Mef2 gene, which is required for the differentiation of all types of muscles. Loss of function of the single Mef2 gene in Drosophila abolishes the expression of contractile protein genes in cardiac, skeletal, and visceral muscle cells but does not affect muscle cell identity, demonstrating the dedication of this factor to muscle differentiation.

Mutation of the GATA gene, pannier, in Drosophila results in an absence of cardioblasts and a decrease in the number of pericardial cells (20). tinman expression is lost in pannier mutants, and ectopic expression of pannier results in the production of supernumerary cardioblasts. Multiple T-box genes function together with tinman and pannier to control cardiac fate, differentiation, and patterning of the dorsal vessel (21, 22). The Drosophila genome encodes a single member of the Hand family of bHLH transcription factors, which is directly regulated by Tinman and Pannier and is required for normal development of the dorsal vessel (23, 24). Autoregulatory and crossregulatory interactions of tinman, Mef2, pannier, T-box, and Hand genes maintain the cardiac phenotype once the network has been activated by upstream inductive signals.

Adding New Units of Structure and Function to the Vertebrate Heart

In vertebrate embryos, cardiac precursor cells are specified in the lateral mesoderm by signals from adjacent tissues, many of which are conserved in organisms ranging from insects to mammals (1, 2). Cardiac progenitors from the primary heart field converge at the ventral midline to form a linear heart tube that resembles, both structurally and functionally, the primitive heart thought to exist in ancestral chordates. Development of the heart tube into the mature multichambered heart requires multiple steps that depend on genetic programs unique to vertebrates and/or amniotes. The heart tube gives rise to the left ventricle of the four-chambered heart, which is believed to represent the ancestral chordate cardiac compartment (13). The right ventricular chamber and outflow tract, later evolutionary advancements, are formed primarily from an adjacent population of precursors, referred to as the secondary or anterior heart field (25–27). Although there is debate as to whether this supplemental cell population represents a separate heart field versus an expanded region of the primary heart field, it is reasonable to conclude that the evolutionary addition of the right ventricle, as a new unit of cardiac structure and function, occurred through the recruitment of a novel population of precursor cells to a preexisting organ, rather than by simply expanding a common field of precursor cells. The hearts of fish and amphibians lack a right ventricle but contain a rudimentary outflow tract, a structure derived from the secondary heart field in mammals. It is currently unclear whether the outflow tract in these organisms is derived from the beginnings of a secondary heart field. It is also conceivable that the secondary heart field was first invented not to provide a new ventricle but simply to increase the mass of the original single ventricle, in which case it could have appeared in evolution before the second ventricle was invented.

At the posterior end of the heart tube, signaling by retinoic acid, a vertebrate invention, establishes atrial identity in cells that would otherwise adopt a ventricular fate (11), thereby conveying positional information along the anterior-posterior axis to chamber-specific genes. In this case, a new signaling pathway was coupled to the ancestral cardiac regulatory network to generate a new structure. Portions of the heart tube that do not become chamber myocardium give rise to the cardiac conduction system through genetic pathways that are also unique to vertebrates.

Later on, the author provides this:

Building Cardiac Complexity by Co-opting New Genetic Networks

The co-option of different upstream inputs by the core cardiac gene network appears to have played an important role in the evolution of the heart. In the tunicate Ciona, the single Mesp gene, encoding a bHLH transcription factor, is expressed in cardiac progenitors and is required for the expression of NK2 and Hand genes (29, 42). Similarly, the two Mesp paralogs in themouse (Mesp1 and -2) are redundantly required for formation of the cardiac mesoderm. In contrast, Mesp is not expressed in precursors of the Drosophila heart, suggesting that Mesp and its regulatory network were recruited to act upstream of the ancestral cardiac gene network during chordate evolution, or that the connection of Mesp to the cardiac network was lost during the evolution of insects.

Varying the upstream inputs to the cardiac regulatory network also provides an explanation for the development of the right ventricular chamber from the secondary heart field. Cardiac muscle cells in both the right and left ventricles rely on the same set of transcription factors for activation of the gene program for cardiomyocyte differentiation and the expression of contractile protein genes, but the upstream inputs into this regulatory network differ in cells derived from the primary and secondary heart fields (Fig. 4A). The evolutionary addition of the secondary heart field required a signaling mechanism to activate the core cardiac transcriptional network. The Isl1 transcription factor, which is expressed specifically in the secondary heart field (26), directly activates the Mef2c gene in this population of cardiac precursor cells (Fig. 4B) (43). In this case, Isl1 was connected to the cardiac regulatory network, possibly through the acquisition of Isl1-dependent enhancer modules by Mef2c and perhaps other core cardiac regulatory genes. Because Isl1 is not cardiac-specific, its initial activation and its actions on downstream targets require combinatorial mechanisms with other factors or epigenetic influences. GATA factors and Nkx2-5, which are expressed in both heart fields and are required for Mef2c expression in the secondary heart field, may serve this role. The forkhead transcription factor Foxh1 also activates Mef2c transcription in the secondary heart field through a separate enhancer and appears to act downstream of Isl1 (44). Mutations in Isl1, Mef2c, or Foxh1 all result in severe cardiac defects that appear to reflect ablation of the secondary heart field and its descendent structures (26, 35, 44), demonstrating the interdependence of these cardiogenic regulators.

These findings suggest that the evolution of the four-chambered heart involved the acquisition of a new set of regulatory inputs into the ancestral cardiac transcription factor genes. Because genes within the core cardiac network cross-regulate and autoregulate their expression, activation of one or a few of the genes in the network may ultimately activate them all, as well as common sets of downstream genes. The regulation of the core set of myogenic transcription factors by different upstream signals in different cardiacmuscle precursor populations is reminiscent of the strategy for skeletal muscle development in which members of the MyoD family are regulated by different upstream signals and transcriptional inputs in different skeletal muscle lineages, thereby contributing to muscle diversity and specialization (45).

Next, we have this paper:

Gene Regulatory Networks For The Development And Evolution Of The Chordate Heart by Yutaka Satou & Nori Satoh, Genes & Development, 20: 2634-2638 (2006)

Gene regulatory networks consisting of subcircuits of transcription factors and intercellular signaling molecules are key to an understanding of the complex mechanisms of animal development and evolution (Davidson and Erwin 2006). One of the most intensively studied genetic networks is that for the formation of the animal heart. Since the discovery of the “tinman” gene (Bodmer 1993) and its vertebrate homolog, Nkx2.5 (Lyons et al. 1995), many genes have been found to be involved in heart development in a wide range of animals, from insects to mammals. Actually, it is well established that a gene circuit consisting of GATA, Nkx, and Hand is evolutionarily highly conserved. This gene circuit constitutes a “kernel,” which is evolutionarily inflexible and performs essential regulatory functions in building a body part (Davidson and Erwin 2006). Analyses of vertebrate heart development revealed that the differentiation of cardiac muscle cells and morphogenesis of the heart are governed by this heart kernel gene regulatory network (Cripps and Olson 2002; Harvey 2002; Buckingham et al. 2005). An important question to be answered about the formation of the heart in vertebrates and other chordates is how this kernel is turned on at the earliest stages of the heart cell specification process to establish the heart field.

Another intriguing question in chordate heart formation is how the dual- or multichambered heart of vertebrates evolved. It is generally believed that the ancestral chordate resembled the present-day ascidian tadpole. The morphogenetic movement of heart precursor cells during ascidian larval development and metamorphosis is reminiscent of those in vertebrates (Davidson and Levine 2003). However, the ascidian tube-like heart lacks chambers. The innovation of the chambered heart was a key event in vertebrate evolution, because the chambered heart generates one-way blood flow with high pressure, a critical requirement for the efficient blood supply of large-body vertebrates.

In this issue of Genes & Development, Davidson et al. (2006) addressed these questions by examining the function of an Ets-containing transcription factor in the tunicate, Ciona intestinalis. They found that Ci-Ets1/2 (because this is one of two Ciona orthologs for vertebrate Ets1 and Ets2 and Drosophila pointed, it was originally called Ci-ets/pointed2) (Yagi et al. 2003) establishes the heart field, probably through an FGF signal acting downstream from Ci-Mesp, a basic helix–loop–helix transcription factor gene required for the initial specification of heart precursor cells (Satou et al. 2004). Targeted inhibition of Ci-Ets1/2 or FGF receptor function blocks heart formation. Moreover, targeted expression of a constitutively active Ci-Ets1/2 causes the expansion of the heart field by forced recruitment of larval tail muscle cells that express Ci-Mesp. Interestingly, this heart field expansion, evoked by the subtle alteration of the heart genetic program, caused a morphological change—that is, to a heart with two compartments.

So, alteration in the expression of one gene in Ciona intestinalis results in a dramatic morphological change, from a single-chambered heart to a two-chambered heart. Hmm. Looks like those biologists know more than they're given credit for by the mythology fetishists, doesn't it?

There's more. Viz:

Mesp, Ets, and FGF signaling cascade in Ciona heart development

Ascidians have an open blood–vascular system, and its blood flow, produced by peristaltic contractions of the heart, is regularly reversed (Ichikawa and Hoshino 1967). The ascidian heart is formed after metamorphosis as a simple tube-like structure with a single-layered myoepithelium that is continuous with a single-layered pericardial wall. It lacks chambers and endocardium. Cell lineage tracing of heart-forming cells reveals that they descend from a pair of blastomeres named B7.5 of the 110- cell stage embryo (Hirano and Nishida 1997). B7.5 also contributes to the anterior tail muscle cells of the tadpole.

The heart regulatory kernel—GATA, Nkx, and Hand—is also conserved in the Ciona embryo. A previous study showed that this highly conserved kernel is under the control of Mesp (Satou et al. 2004). Ciona Mesp, the sole ortholog of vertebrate Mesp1 and Mesp2, is expressed in B7.5 blastomeres where it regulates Nkx, HAND, and NoTrlc (a nonorthologous gene similar to vertebrate Hand, and also called Hand-like). Knockdown of Mesp results in failure of proper specification and migration of the heart precursors (Satou et al. 2004). In mice, Mesp is expressed in mesodermal cells including the region that forms the heart; no heart is formed in Mesp1 and Mesp2 double knockout mice (Kitajima et al. 2000). There is no indication that Mesp is involved in heart formation in nonchordate animals. Thus, Mesp provides a critical link between the mesoderm and heart field in chordates (Fig. 1). However, in both ascidian and mouse embryos, only some of the cells that express Mesp give rise to the heart. How is this achieved?

Davidson et al. (2006) have addressed this important question. By using elegant confocal imaging and transient transgenesis in Ciona embryos, they showed that Ci-Ets1/2, a transcriptional effector of receptor tyrosine kinase (RTK) signaling, acts downstream from Mesp to establish the heart field. Mesp expression begins at the 110-cell stage (immediately before gastrulation) in B7.5 and persists in B7.5-derived progenitors of the heart and larval tail muscles (Satou et al. 2004). Ci-Ets1/2 expression initiates during gastrulation in four cells descended from two Mesp-expressing founder cells. After gastrulation, these cells divide asymmetrically, and the smaller rostral daughter cells exhibit RTK activation and form the heart progenitors while the larger caudal daughters give rise to the larval tail muscle. Inhibition of RTK signaling and targeted inhibition of Ci-Ets1/2 function block heart specification. Conversely, targeted expression of a constitutively active form of Ci-Ets1/2 causes a fate change of the larger caudal daughters to form heart
cells (Davidson et al. 2006).

Later on, the authors provide this:

Insight into an evolutionary change in morphology evoked by changes in the genetic program

Invertebrate chordates have nonchambered hearts while all extant vertebrates have hearts with two or more chambers (Moorman and Christoffels 2003). As mentioned above, the ascidian heart is a simple tube-like organ, while the vertebrate heart has chambers partitioned by septa, and the chambers sequentially contract under the control of the conduction system. It is highly likely that vertebrates evolved the dual-chambered heart through modification of the gene regulatory networks responsible for heart formation in ancestral chordates. Davidson et al. (2006) have also presented a suggestive result on the evolution of the vertebrate multichambered heart.

All Mesp-expressing cells of Ciona embryos (half normally form larval tail muscle cells) were converted into heart fate by targeted expression of constitutively activated Ci-Ets1/2. This treatment resulted in a doubling of the heart field. Some of the resulting juveniles have a heart with two compartments that beat sometimes independently and sometimes in a coordinated fashion (see Fig. 7 in Davidson et al. 2006). This mutant heart clearly needs to be further characterized morphologically, anatomically, developmentally and electrophysiologically. This two-compartment heart should lack a conduction system and other accessory structures characteristic of vertebrate hearts, like valves and septa. The mutant heart is expected to beat by peristalsis, rather than the sequential contraction of two compartments. It also probably lacks the dynamic suction pumping seen in the heart tube appearing at the beginning of vertebrate heart development (Forouhar et al. 2006). Nevertheless, the hypothesis proposed by Davidson et al. (2006) presents a new possibility for our understanding of evolution.

The hypothesis includes two major points. First, increasing the number of primordial heart cells can occur by recruitment of competent cells that normally follow an alternative fate, rather than by excess cell divisions. Excess cell divisions do not expand the net volume of cells following a given fate, whereas cell recruitment does. In the former case, if newly divided cells form a new structure, then the size of the original tissue must be reduced. This could impair function. In contrast, recruitment through cell fate transformation can add new components to an existing structure without impairing its function. In addition, recruitment can be obtained through subtle changes in a genetic program, such as altered expression of FGF9/16/20. It is therefore possible that this strategy is a general pathway of evolutionary change.

So, a change in the expression of one gene, resulted in the emergence of a two-chambered heart in an organism that previously only had a single-chambered heart, by the recruitment of neighbouring embryonic cells that usually have a different fate.

I could find more papers in a similar vein if I wished, but these were the ones most quickly available to me.

Moving on ...

This system portraits [sic] what is known as Irreducible Complexity. None of the components in this system could exist without the other. So which one "evolved" first?

HA HA HA HA HA HA HA HA!!!!

If you think that the caricature of "irreducible complexity" as peddled by that charlatan Behe counts for anything, you really are ignorant. Because, wait for it, "irreducible complexity" wasn't first proposed by Behe, but , who first presented the concept way back in 1918, and who furthermore presented the concept NOT as a "problem" for evolutionary biology, but as a natural outcome of evolutionary processes. In short, evolutionary biologists have known that Behe's canards on the subject were canards sixty years before Behe was born.

The relevant scientific paper in which Müller presented the genuine concept of "irreducible complexity" is this one:

Genetic Variability, Twin Hybrids and Constant hybrids in a Case of Balanced Lethal Factors by Hermann Joseph Müller, Genetics, 3(5): 422-499 (1918) [Original paper downloadable in full from here]

I shall quote directly from that paper for your convenience, highlighting the relevant parts in blue (bottom of page 464 to top of page 465 in original paper):

Most present-day animals are the result of a long process of evolution, in which at least thousands of mutations must have taken place. Each new mutant in turn must have derived its survival value from the effect upon which it produced upon the 'reaction system' that had been brought into being by the many previously formed factors in cooperation; thus, a complicated machine was gradually built up whose effective working was dependent upon the interlocking action of very numerous different elementary parts or factors, and many of the characters and factors which, when new, were originally merely an asset finally became necessary because other necessary characters and factors had subsequently become changed so as to be dependent upon the former. It must result, in consequence, that a dropping out of, or even a slight change in any one of these parts is very likely to disturb fatally the whole machinery.

In other words, "irreducible complexity" was arrived at by Müller before Behe was born and was posited by Müller not as a problem for evolution, but as a natural outcome of evolutionary processes. The so-called "Müllerian Two Step" is summarised succinctly as follows:

[1] Add a component;

[2] Make it necessary.

This was placed upon a rigorous footing by Müller himself, along with others such as Fisher, by the 1930s, and so Behe didn't even find a gap for his purported god to fit into. Biologists have known that Behe's "irreducible complexity" nonsense has been precisely that - nonsense - for a minimum of six decades. Indeed, the community of evolutionary biologists have a term to describe the Müllerian Two Step in more formal language, namely 'bricolage'.

All Behe did was coin a soundbite, and then present this duplicitously as if it constitutes a "problem" for evolutionary biology, when it does nothing of the sort. So-called "irreducibly complex" systems were postulated by Müller in 1918 to be a natural outcome of evolutionary processes, as the section of his paper I quoted above establishes. Behe simply erected a blind assertion (one of many, I might add, that were all refuted during the Dover Trial), to the effect that because he couldn't work out how testable natural processes achieved the end result, this purportedly meant that no testable natural process could achieve the end result, and therefore, a magic man was purportedly needed. Those scientific papers I presented in that other post destroy this myth utterly. Behe's sad little canard was known to be a canard before the sperm met the egg to form him.

So if you think no one here has dealt with the canard of "irreducible complexity" sensu Behe before, you're sadly mistaken. I subjected this canard to demolition along the above lines, getting on for twelve years ago over at the old Richard Dawkins Forums, and no IDist has ever produced anything other than worthless apologetic fabrications in order to try and address said demolition.

Once again, game over for your canards.

Moving on ...

Back to the evidence. A building is the evidence for the builder, a painting is the evidence for the painter,

Really?

Guess what, boy? I have a challenge for you. If you think, naively and stupidly as you do, that it's purportedly "obvious" when something is fabricated, I've a little test for you, which NO mythology fanboy has ever even dared to undertake when presented with it, let alone pass it. I'm attaching a nice little image to this post, of some rocks. ONE of those rocks is a Palaeolithic stone tool, while the rest are simply everyday rocks shaped by the everyday forces of nature. Can you tell the human artefact from the non-artefacts from that picture? I'm willing to bet you can't, and I'll enjoy watching you fail if you try.

Plus, there are many regular structures in existence, that are not the product of human, or for that matter, any other sentient entities. The Richat Structure in the Sahara desert was produced by mindless erosion. The Pamukkale Formation was produced by mindless precipitation of minerals from water. Fingal's Cave was produced by a mindless basalt lava flow. The Cave of the Crytsals was produced by mindless precipitation.

Just because you're too stupid to understand how testable natural processes can produce entities of this sort, doesn't validate your imaginary cartoon magic man.

Oh for that matter, we also have the Oklo fossil nuclear reactors to bring to the table. Yes, that's right, we have evidence that nuclear reactions occurred in natural rock formations 1.7 billion years ago, long before there existed humans to build nuclear reactors. Anomalous isotope ratios allowed for the detection of these fossil reactors, when material was being checked for nuclear proliferation compliance.

And, of course, the evidence for the biosphere being the product of yet more testable natural processes, is documented in around 1½ million peer reviewed scientific papers, including tens of thousands of papers providing direct experimental test and validation of relevant evolutionary postulates. Don't even think of asserting otherwise, unless you want to unleash the avalanche.

creation is the evidence for The Creator.

Bollocks.

First of all, you appear not to have noticed that testable natural processes have been found to be sufficient to account for vast classes of entities and interactions, including [1] entities and interactions that mythology fanboys like you, oh-so-confidently asserted in the past needed an invisible magic man to "explain" them, and [2] entites and interactions that the authors of your sad mythology were incapable of even fantasising about.

Here's a clue for you. The piss-stained Bronze Age incels who scribbled your sad little mythology, were not only incapable of counting correctly the number of legs that an insect possesses, and asserted within their diseased scribblings that genetics was purportedly controlled by coloured sticks, but they knew nothing of the existence of at least four major continental land masses on this planet. If as I suspect, you're residing in the USA, then you're residing on one of those land masses, and this should be a serious source of embarrassment to you. Apparently your cartoon magic man forgot to tell his goat herder ghostwriters salient features of Planet Earth, let alone anything beyond.

Furthermore, the semi-literate goat herders who scribbled your sad mythology, underestimated the age of the universe by at least seven orders of magnitude, and its size by at least nine orders of magnitude. Which means that your attachment thereto, from the standpoint of genuine knowledge, is farcical.

Second, I've already covered at length, the manner in which testable natural processes are perfectly capable of producing artefacts that look "designed" to the uneducated and gullible. The evidence for testable natural processes being responsible for the universe and its contents is present by the supertanker load, in upwards of five million peer reviewed papers published in a vast swathe of scientific disciplines.

I have already shared this. I have not ignored you, but have given you evidence. You didn't want to see it.

What you've presented here isn't "evidence", it's the usual mythology fanboy blind assertions masquerading as such. Once again, your rectally extracted apologetic fabrications only provide evidence of your inadequacy.

To say that everything just randomly fits together and formed itself is like saying that you can put all the parts of a watch into a box, and shake them up and that they will randomly fit themselves together into a functioning watch which also just so happened to set itself to the right time.

And of course, no one who paid attention in class, least of all the requisite research scientists providing the peer reviewed papers containing the evidence for testable natural processes, asserts this fatuous caricature of scientific thinking, which is a duplicitous creationist fabrication.

Oh by the way, there are scientific papers documenting self-assembly of relevant structures, if you bother to look for them. Arising from nothing other than electrostatic forces and chemical reactions.

Again, I have not lied to you, Sheldon. I have given you evidence. You have lied to yourself.

I'm sure Sheldon will subject this latest assertion of yours to the carpet bombing it deserves. On the other hand, what about the lies you've been telling yourself above, now duly exposed as such?

Moving on ...

If atheists do not believe God exists, then who do they say is responsible for creation?

Now a "who", but a "what". Try testable natural processes.

If not God, the only other possibility would be said, "nothing," being that creation could not create itself.

Excuse me, but I DEMOLISHED YOUR PREVIOUS ERECTION OF THE DUPLICITOUS "ATHEISTS THINK THE UNIVERSE CAME FROM NOTHING" LIES AND BULLSHIT IN YOUR PREVIOUS THREAD. Courtesy of this post, within which I provided a six step rebuttal of your canard.

But I'm used to the combination of intellectual indolence and duplicity that is a well-documented part of the creationist aetiology.

Simple question for you ... ARE YOU GOING TO STOP POSTING LIES?

As for that other possibility, try, once again ... TESTABLE NATURAL PROCESSES.

Cog, I answered that question as a reply to Sheldon in one of the comments above. I was asked not to copy and paste, so you will have to go and read it there.

No you didn't. Blind assertions and ex recto fabrications do not equal "evidence", except as evidence for your inadequacy.

I notice you've been avoiding my posts the way Kent Hovind dodged paying taxes. I suspect others are drawing the requisite conclusions from this.

Comfort - ...cause an atheist actually believes nothing created everything...

Is that statement from Mr. Comfort accurate?
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Clearly it isn't accurate; and I don't think it takes a big stretch to believe that Mr. Comfort knows it isn't accurate. And I find it hard to believe he just misspoke, because the video was edited to include that statement in the final product. Why do you think that is?

Is it because Ray Comfort is a lying sack of shit? A duplicitous creatard with all the integrity of a politician on polling day, or a televangelist in full money grabbing flow.