Posted: Feb 25, 2014 4:51 pm
by Calilasseia
questioner121 wrote:
Frank Merton wrote:I take it questioner121's point is that we can't travel in time to see evolution and therefore we can't know it happened. Do I have that right? Is that really the position?

We can't travel back in time to see what caused the trilobites to die off or the evolution of primates to humans or confirm the age of the earth.

Irrelevant apologetic fabrication. Because, oh, wait for it, the relevant physical processes left behind persistent physical evidence of their occurring. Said evidence is what tells us that these events took place. Another elementary concept you appear not to understand.

As for the age of the Earth, I refer you to this. Read it and learn something.

questioner121 wrote:What we have today is evidence which can be interpreted in different ways

Oh no, it's the creationist "interpretations" canard again ... yawn ...

The "assumptions" canard (with "interpretation" side salad).

This is a frequent favourite with creationists, and usually erected for the purpose of attempting to hand-wave away valid science when it happens not to genuflect before their ideological presuppositions. As I have stated earlier, science is in the business of testing assumptions and presuppositions to destruction. As an example of destroying creationist apologetics with respect to this canard, I point interested readers to this post, where I destroyed the lies of the laughably named "Answers in Genesis" with respect to their assertion that 14C dating was based upon "assumptions". I've also trashed this canard in detail with respect to radionuclide dating as a whole, so don't even try to go down that road. Likewise, if you try to erect this canard with respect to other valid scientific theories, you will be regarded as dishonest.

Another favourite piece of creationist mendacity is the "interpretation" assertion, which creationist erect for the purpose of suggesting that scientists force-fit data to presuppositions. Apart from the fact that this is manifestly false, it is also defamatory, and a direct slur on the integrity of thousands of honest, hard working scientists, who strive conscientiously and assiduously to ensure that conclusions drawn from real world observational data are robust conclusions to draw. This slur, of course, is yet another example of blatant projection on the part of creationists, who manifestly operate on the basis of presupposition themselves, and appear to be incapable of imagining the very existence of a means of determining substantive knowledge about the world that does not rely upon presupposition. Well, I have news for you. Science does NOT rely upon "presupposition". Indeed, scientists have expended considerable intellectual effort in the direction of ensuring that the conclusions they arrive at are rigorously supported by the data that they present in their published papers. There exists much discourse in the scientific literature on the subject of avoiding fallacious or weak arguments, including much sterling work by people such as Ronald Fisher, who sought during their careers to bring rigour to the use of statistical inference in the physical and life sciences. Indeed, Fisher was responsible for inventing the technique of analysis of variance, which is one of the prime tools used in empirical science with respect to experimental data, and Fisher expended much effort ensuring that inferences drawn using that technique were proper inferences to draw.

Basically, there is only one "interpretation" of the data that matters to scientists, and that is whatever interpretation is supported by reality. Learn this lesson quickly, unless you wish to be regarded as discoursively dishonest on a grand scale.

questioner121 wrote:and unproven for the explanations we derive for them.

Bullshit. Apart from your failure to distinguish between proof and evidential support, the evidence clearly points to the explanations presented to you. First, I'll deal with your failure to understand the difference between proof and evidential support, viz:

Learn the distinction between proof and evidential support.

This is something that supernaturalists never tire of failing to understand, so once and for all, I shall present the distinction here.

Proof is a formal procedure in pure mathematics, and only applicable to that discipline. Proof consists of applying, in an error-free manner, well-defined rules of inference to the axioms of a given mathematical system in order to produce theorems, and thence recursively to those theorems to produce more theorems.

Evidential support consists of providing empirical demonstrations that a given set of postulates is in accord with observational reality. This is the process that is used in the physical sciences in order to build scientific theories. Postulates that are NOT in accord with observational reality are discarded.

If you cannot exercise the basic level of intellectual effort required to learn this simple distinction, or worse still, erect fatuous nonsense about "proving" a scientific theory (especially if "prove" is mis-spelt with two 'o's), then expect your posts to be treated as a free fire zone for scathing and withering derision.

I also refer you to my exposition on the "assumptions" and "interpretations" canard above.

questioner121 wrote:For example, the evidence for common ancestry is not based on observations of populations interbreeding with one another it's based from traits.

Already dealt with this in previous posts. Apparently you missed this. I covered this both here, viz:

Here is what actually happens:

[1] Organisms are observed reproducing, Those organisms are therefore considered to be part of the same species.

[2] Genetic data is collected from those organisms (and their offspring), allowing us to determine such details as inheritance mechanisms. A process that started back in the 19th century with Gregor Mendel.

[3] Given that we have hard evidence for inheritance in this manner, and zero evidence for other processes (such as magic conjuring tricks by an invisible magic man), it is natural to conclude that closely related species acquired their shared anatomical features from a common ancestor.

[4] At this point, we look for ways of testing this hypothesis. One such test being to observe speciation taking place. Which has been done. Documentation of speciation events is voluminous.

[5] At this point, we also ask whether or not the patterns of inheritance we see are consistent with the common ancestry hypothesis. This test has also been performed, not least by Douglas Theobald, who compared ]i]different[/i] ancestry models with the genetic data, and established in his paper on the subject, that the universal common ancestor model is a whopping 102,860 times more probable than other ancestry models.

In other words, the data says common ancestry is valid. Game over.

and more briefly here, viz:

You do realise that biologists have observed reproduction in everything from protists to primates? That's a pretty broad remit.

In that latter post, I also provided an in depth explanation of why the creationist "I've never seen a dog give birth to a cat" canard is precisely that. Did you bother reading this?

questioner121 wrote:However the non believers have been deluded into thinking otherwise.

Bullshit. Oh wait, we have enough evidence of traits being inherited from reproductive ancestors. Try your family photo album for starters.

Oh, and there's also the little matter that not only are working genes inherited from reproductive ancestors, but broken genes as well, such as the broken gene for gulonolactase in hominid primates, which results in said primates being unable to synthesise vitamin C. There's also a broken gulonolactase gene in the guinea pig lineage, but, oh wait, in that lineage, the gene is broken in a different manner. Whilst the broken gulonolactase genes in humans and chimpanzees are broken in exactly the same place.

Then of course there's endogenous retroviral insertions. Endogenous retroviral insertions, to give them their full title, occur when retroviruses affect germ cells in an organism, but, in a sense, fail to clean up after themselves. In order to explain why I describe ERVs in this manner, I need to provide a little exposition on how retroviruses work.

A retrovirus is a virus that uses RNA as its genetic material. The term "retrovirus" itself arises from this fact, because the mechanism by which a retrovirus operates, runs in direct opposition to the sequence of events that was once labelled "the central dogma of molecular biology". The familiar sequence, that operates in organisms such as ourselves, consists of reading from a DNA strand, producing messenger RNA strands from the read information, then using those messenger RNAs to direct protein synthesis. In short, that sequence can be represented as DNA -> RNA -> Proteins. Retroviruses run the sequence backwards to a certain extent, using a special enzyme called reverse transcriptase, which takes the RNA genome of the virus, and creates a DNA copy. That DNA copy is then spliced into the DNA of the infected cell, in order to hijack the cell's machinery to make more copies of the virus. A pretty sneaky way of getting yourself reproduced.

The trouble here, is that the retroviruses in question don't destroy the host cell. Many viruses do destroy the host cell, once enough daughter viruses have been produced - the cell in this case bursts open and dies, releasing the thousands of daughter viruses. With retroviruses, on the other hand, the cell doesn't burst open (a process known technically as 'lysis'), but remains intact, the daughter viruses being shed via a 'budding' process through the cell wall. HIV is an example of a retrovirus operating in this manner, and this is one of the reasons HIV is so insidious - an infected cell can go on producing HIV viruses for a long time, once the viral genome has been spliced into the cell's genome.

Now, at this point, you can see why I described retroviral insertions into a genome using the phrase "fail to clean up after themselves" - because the viruses leave behind copies of their genome in infected cells. If the retrovirus is shut down by the immune system, then what happens sometimes is that the inserted viral genome is silenced, by appropriate enzymes acting on the cell's DNA. But, it isn't removed from the cell's DNA. That retroviral genome remains in place, but inactive, and there exist a number of processes that can lead to this silencing, such as the insertion of stop codons at the start of the gene sequence, that result in that gene sequence not being read and translated. The actual molecular biology would take pages to describe in full, but for now, we can simply accept that cells have silencing mechanisms, that can stop unwanted genes from being expressed.

Now, if a retrovirus inserts its genome into a germ cell (i.e., a cell responsible for the synthesis of reproductive egg and sperm cells), and that genome is then silenced, that silenced copy can be passed on to those egg and sperm cells, and thence to the affected organism's offspring. When the genome of the offspring is then sequenced, those silenced genes turn up in the sequence being read.

Now, an additional point to bear in mind here, is this: retroviruses do not exhibit any major preference for particular parts of the host cell's genome. They will insert their genetic material more or less anywhere in the host's DNA, provided that said insertion point results in the viral genome being read, translated, and new daughter viruses being produced. So, a retroviral insertion can occur more or less anywhere in a host genome. In the case of humans, that genome is 3.5 billion base pairs in size, so there's a LOT of options for a retrovirus. There will be some restriction on the choice of insertion point, because some insertion points will simply not work, but there will be a large number of possible insertion points that will work, and the retrovirus will choose whichever happens to be the most convenient to use when it turns up. As a result, retorviral insertions are effectively random events.

However, I just described above, how silenced retroviral insertions can be inherited, and passed on down to future generations. Those silenced retroviral insertions, give or take a mutation here or there due to genetic drift, will persist in that lineage. If that lineage gives rise, further down the line, to two new species, then both of those species will inherit that retorviral insertion, which will thus become a marker of common ancestry for those two species.

To illustrate this process in action, I constructed a nice little hypothetical family tree, which I illustrate below:

ERV Inheritance Representation.jpg

ERV Inheritance Representation.jpg (188.57 KiB) Viewed 878 times

In that diagram, lineage A acquires 3 random retroviral insertions into its genome. That lineage then gives rise to two new lineages, A1 and A2, which inherit those insertions. Those two lineages then acquire their own insertions, different ones in each case, and those lineages each give rise to two new lineages of their own, namely A11, A12, A21 and A22. These lineages then acquire some more insertions, and pass these on to the new lineages A111, A112, A121, A122, A211, A212, A221 and A222. The point being, that at each stage, the new lineages inherit whatever insertions occurred in their ancestors. So, even if they acquire new ones, their ancestry will be traceable, by noting which lineages share key collections of retroviral insertions.

Now, for two distinct lineages, that are not connected by common ancestry, to share a given retroviral insertion in the same place in the genome, is an extremely low probability event. After all, each insertion is effectively random, and each retrovirus, when it performs its insertion, has thousands, if not millions, of options. If our retrovirus has a million options for insertion in two genomes, then the probability of that retrovirus independently inserting itself into the exact same place in those two genomes, is 10-12 - a pretty small probability. For two different retroviruses to perform the same trick, we're looking at a probability of 10-24, and for three retroviruses to perform the same trick, we're looking at a probability of 10-36, in our hypothetical instance above. So, an examination of lineage A111 and A112 above, would result in the discovery that those two lineages shared no less than nine identical retroviral insertions. The probabiliy that nine retroviruses independently inserted themselves into those genomes in the same places in those two lineages, is thus 10-112, an astronomically tiny probability. But, the probability of those insertions appearing in those lineages, as a result of inheriting them from past ancestors, is precisely 1. I've just illustrated the family tree outlining this.

As a consequence, one of the checks performed to determine common ancestry of humans and chimpanzees, was to check if the two lineages shared any identical retroviral insertions. It turns out that there are no less than sixteen of them. Now, the probability of those insertions appearing in humans and chimpanzees as a result of independent insertion events is absurdly tiny. Even if you only assume that the retroviruses had a million insertion options (and in the case of the human and chimpanzee genomes, they had a lot more than that), then the probability of sixteen identical insertions taking place independently, is an excruciatingly tiny 10-192. Put it this way, this is about the probability of you being the impact point, on a specific day in the year, for a 10Km meteorite. Since 10Km meteorites aren't raining down on us in large numbers (we'd be pretty much fucked if they were!), this puts matters into perspective. On the other hand, the probability of humans and chimpanzees acquiring those insertions from a common ancestor, is precisely 1, courtesy of the basic way in which inheritance works.

So, the idea that humans and chimpanzees were "separately created" is a non-starter in the light of those figures. And, people who want to erect the "design" assertion, then have the problem of answering another awkward question. Namely, why did their asserted "designer" choose to insert wholly useless pieces of DNA into the two genomes, in precisely the manner expected to appear from inheritance via a common ancestor? To quote the late Bill Hicks, does this mean that the "designer" is fucking with our heads?. As evolutionary biologist Ken Miller, who happens to be a Catholic, said "I happen to believe in a 'designer' in the most general sense, but NOT a deceptive one".

Moving on ...

questioner121 wrote:
ADParker wrote:The evidence for common ancestry is based on observations of species breeding and speciating etc.,
of "traits",
of ring species demonstrating how one gene-pool can 'naturally' split into two,
of genetic comparisons (the same ones that are used to identify suspects/victims and familial relationships like parentage - because it can be used to that level of precision),
of geological and temporal dispersal of living and fossilized organism,
Endogenous retroviruses (where they are placed etc.),
etc. etc...

And all of it fits together so beautifully into the "universal common ancestor " model that it would be just be perverse for someone to understand that evidence and still believe it otherwise
If it isn't true then it looks like something has tried extremely hard to make it look true. :lol:

Here is where you're missing the important point.

He isn't. He provided seven different lines of evidence, all leading to the same conclusion. Or did you fail to notice this?

questioner121 wrote:The evidence for common ancestry is missing observations of one species evolving into another entirely different (for example primate to human or theropod to bird) one via reproduction.

Lie, plain and simple. Oh wait, I covered the whole business of nested clades here. Look, once and for all, drop the farcical "transforming into something else" nonsense, which apart from being another creationist fabrication bearing no resemblance to actual evolutionary postulates, based upon a woefully ignorant view of taxonomy, ignores the fact that Linnaeus introduced nested clades in his classification system a century before Darwin wrote a single word on evolution. Quite simply, humans are primates, and birds are theropod dinosaurs. Organisms don't leave the clade containing their ancestors, just as you don't leave the family containing yours. What part of this elementary understanding of inheritance eludes you?

questioner121 wrote:To fill in the missing gap via extrapolating the observations is wrong in this case due to the unpredictability of nature.

Wrong. Oh wait, once again, we have persistent physical evidence supporting the relevant postulates. Not only do we have evidence from molecular phylogeny (which, incidentally, would be impossible if organisms didn't inherit traits in the standard manner), but we also have large numbers of fossils of organisms exhibiting the relevant morphological transitions. I'm aware of something like 16 of these from the theropod lineage alone. Oh, you might also want to ask yourself why numerous bird lineages still contain genes for the production of reptilian teeth. A relevant paper is this one:

The Development Of Archosaurian First-Generation Teeth In A Chicken Mutant by Matthew P. Harris, Sean M. Hasso, Mark J. W. Ferguson and Joun F. Fallon, Current Biology, 16: 371-377 (21st February 2006)

Here's the opening of the paper:

Harris [i]et al[/i], 2006 wrote:Summary

Modern birds do not have teeth. Rather, they develop a specialized keratinized structure, called the rhamphotheca, that covers the mandible, maxillae, and premaxillae. Although recombination studies have shown that the avian epidermis can respond to tooth-inductive cues from mouse or lizard oral mesenchyme and participate in tooth formation [1, 2], attempts to initiate tooth development de novo in birds have failed. Here, we describe the formation of teeth in the talpid2 chicken mutant, including the developmental processes and early molecular changes associated with the formation of teeth. Additionally, we show recapitulation of the early events seen in talpid2 after in vivo activation of β-catenin in wild-type embryos. We compare the formation of teeth in the talpid2 mutant with that in the alligator and show the formation of decidedly archosaurian (crocodilian) first-generation teeth in an avian embryo. The formation of teeth in the mutant is coupled with alterations in the specification of the oral/aboral boundary of the jaw. We propose an epigenetic model of the developmental modification of dentition in avian evolution; in this model, changes in the relative position of a lateral signaling center over competent odontogenic mesenchyme led to loss of teeth in avians while maintaining tooth developmental potential.

Results and Discussion

Early dinosaurian ancestors of birds (avialan and nonavialan theropods [3]) possessed conical teeth homologous to those of their reptilian ancestors; however, avian teeth were lost at least 70–80 million years ago. In addition, teeth have been independently lost several times within nonavialan theropods, avialans, and chelonians; this loss is correlated with the formation of the horny, keratinized epithelium and the beak [4–6]. In the epidermis of embryonic birds, there remains a transient thickening that is comparable to the early formation of the dental lamina in the mouse [7, 8]; this structure regresses, and invaginations associated with tooth formation do not form. However, the avian oral epithelium has the developmental capacity to initiate tooth developmental programs with underlying grafts of non-avian oral ectomesenchyme [1, 2] as well as avian mesenchyme competent to form integumentary appendages [8]. Additionally, the avian mandibular mesenchyme can respond to inductive signals from mouse mandibular epithelium and form tooth-like structures with differentiation of pre-dentine [9]. This demonstration of dormant developmental programs revealed in recombination experiments emphasized the study of experimental atavisms, such as ‘‘Hen’s Teeth,’’ in understanding the role of development in evolutionary change [1, 10–12]. Given the latent capacity of the chicken mandibular epidermis to participate in tooth morphogenesis, the problem remains as to what extent tooth programs are maintained in birds in an in vivo context of the developing jaw andhow this relates to the loss of avian teeth in evolution.

Here, we describe the first evidence of tooth developmental programs and morphology initiated in an extant bird as a result of either mutation or experimentation and, importantly, without xenoplastic tissue grafts or tissue manipulation. Because birds and mammals evolved in parallel (avian and mammalian lineages shared a common ancestor in the early amniotes at least 300 million years ago), the relevant comparison for avian tooth developmental programs is within the archosaurs, with crocodilians, the closest living relative of birds. Among other things, crocodilian tooth development, e.g., in alligators, differs from that of mammals in that the formation of first-generation teeth is initiated as an evagination of the integument rather than an invagination of the epithelium [13]. The subsequent generations of tooth formation in the alligator form epithelial invaginations as in mammals. This pattern of tooth formation is thought to be similar for other reptiles [13]. Our analysis of the developmental programs of tooth formation of the talpid2 (ta2) chicken shows similarity with the formation of first-generation crocodilian teeth. In addition, we propose that the oral/aboral boundary establishes a signaling center that, depending on its apposition to underlying competent mesenchyme, controls the initiation and suppression of teeth.

So, the authors of this paper alighted upon a chicken mutant in which formation of teeth takes place, with those teeth possessing manifest archosaurian morphology. Indeed, the teeth formed bore sufficient morphological resemblance to those of Alligator mississippiensis to render any alternative interpretation untenable.

Moving on to the details of the paper:

Harris [i]et al[/i], 2006 wrote:Developmental Specification of Teeth in ta2

ta2 is an autosomal recessive mutation that affects the development of several organ systems in the chick [14]. We observed the formation of integumentary outgrowths on the developing jaw of 14- to 16-day-old ta2 embryos (E14–E16). These structures were only formed in close association with the lateral boundary of the oral cavity and were found at the distal boundary of the jaw (Figures 1B and 1D). On the mandible, these structures were equally spaced in a line positioned more centrally in the oral cavity than the formation of the distal lamellae of the wild-type chick jaw (compare Figures 1A and 1B). The maxilla, deformed in the mutant, showed similar outgrowths clumped at the altered distal margin of the jaw (Figure 1D).

ta2 embryos rarely survive past E12. However, we were able to isolate several near-hatching stages (n = 5). The loss of the rhamphotheca during preparation for skeletal analysis in several of these specimens uncovered the formation of a set of conical, saber-shaped outgrowths from the distal mandible; these outgrowths had previously been hidden by the horny epidermis of the beak (Figures 1E and 1F; 100%, n = 3). Underlying these outgrowths, remodelling of the mandible can be seen (Figures 1E and 1F). Furthermore, sectioning of near-hatching-staged ta2 jaws with an intact rhamphotheca revealed the formation of a lamina at the lateral oral/aboral boundary (Figures 1G and 1H). At the base of the lamina, there was evidence of differentiation of the surface epithelial cells away from the normal keratinized squamous morphology (Figure 1H).

Histological analysis of the outgrowths of E14 ta2 embryos indicated a shift of the oral/aboral boundary when compared to wild-type siblings, as marked by specific epithelial histology of the horny stratified squamous epithelium of the aboral epithelium compared to the stratified squamous, nonkeratinizing, epithelium of the oral cavity (dotted line, Figures 1I–1N). The formation of paired outgrowths occurred at this new boundary. The morphology and histology of these outgrowths, including the organization of the dental mesenchyme and vascularization, are identical to those of the early evaginations seen in the development of first-generation teeth of the alligator (Figures 1K–1P, and see [13]). Neither the chick nor alligator dental structures make enamel, and there was no evidence of dentine in either [13]. However, the outgrowths in ta2 show a circumferential layer of cells that resemble early odontoblasts and show evidence of matrix deposition (Figures 1K–1N; see also [15]). These data suggest that the ta2 chick is capable of forming early dental structures anatomically similar to the first-generation teeth of the alligator.

Initiation of Latent Tooth Developmental Programs in ta2

To compare the initial developmental programs of tooth formation in the alligator and chick, we looked at the expression of sonic hedgehog (shh) in comparably staged embryos of the two species. Shh is expressed in the early odontogenic epithelium of vertebrate teeth [16, 17] and is necessary for tooth formation in the mouse [18, 19]. Alligators show distinct round foci of shh expression in forming tooth anlagen connected together by expression that may mark the forming lamina (Figures 2A and 2D). In ta2, similar expression of shh is seen in the oral appendages of E10-staged embryos (Figures 2B and 2E). The expression of shh along the oral/aboral junction and teeth primordia is analogous in both alligators and ta2 embryos (arrows; Figures 2A, 2D, 2B, and 2E). ta2 wild-type siblings showed only diffuse shh expression in the lateral, aboral epidermis (Figures 2C and 2F).

In addition to shh expression, we analyzed the expression of other tooth developmental genes, necessary for tooth formation in the mouse, that are conserved in vertebrate tooth development [16]. patched (ptc) expression is a sensitive marker for shh signalling. Analysis of ptc expression demonstrated the activation of shh signaling in the lateral oral/aboral boundary and punctate foci at the distal margins of the jaw (Figures 2G and 2J). We also analyzed the expression of pitx2, a marker of odontogenic epithelium [20, 21], as well as that of bone morphogenetic protein 4 (bmp4), which is expressed in early odontogenic epithelium but is expressed later and primarily in the mesenchyme [22]. In ta2, pitx2 is expressed in punctate foci on the oral epithelium concomitantly with shh and ptc (Figures 2H and 2K); this expression is in stark contrast with that in the wild-type sibling (Figures 2H and 2K, inset). It is noteworthy that pitx2 is not known to be expressed during the formation of other integumentary appendages and thus is a putative specific marker for tooth formation (see below). Chen et al. [8] noted the absence of bmp4 expression laterally in the chick when compared to the mouse and postulated that this may be a limiting factor in the ability to make teeth in the bird. Consistent with this view, we show that bmp4 is regionally expressed in the mutant around presumptive tooth placodes in the maxilla (Figure 2I) and is upregulated in the distal mandible and lateral aspects of the lower jaw, where tooth formation is seen in older embryos (arrows, Figure 2L). These data indicate that tooth-specific developmental programs are being activated in the ta2 chicken.

Early Disruption of Lateral-Boundary Formation in the Developing Oral Integument in ta2

The affected gene in ta2 is unknown. However, the effect of the ta2 gene on limb development has been shown to be due to an activation of the shh signaling pathway, resulting in an inappropriate activation of shh downstream genes in the absence of increased shh expression [23]. Gene expression analysis in ta2 facial primordia indicates that similar misregulation of shh signaling is occurring there as well [24]. Current work in mouse suggests that early shh signaling in the epidermis may play a role in positioning the sites of tooth formation on the oral epidermis [25, 26]. In addition, the antagonistic signaling function between fibroblast growth factor 8 (fgf8) and bmp4 in the early frontonasal and branchial arch ectoderm is thought to function in a similar manner [27]; how these signaling pathways are integrated remains to be determined.

Given the observed change in the lateral boundary of the jaw seen in histological sections of ta2, we investigated the regulation of early oral/aboral markers in developing facial prominences to see whether early developmental specification of tooth development may be altered in the mutant. Expression of fgf8 in Hamburger and Hamilton stage 21 (s21, [28]) ta2 embryos showed ectopic expression in the presumptive oral cavity and forming maxillary and mandibular processes (Figures 3A–3D). Similarly, the expression of bmp4 outlines a smaller region of the frontonasal ectoderm and coincides with changes in the fgf8 expression domain in the mutant (Figures 3E and 3F). As noted above, in the mouse, pitx2 is an early marker for odontogenic epithelium, in which pitx2 expression straddles the forming oral/aboral boundary as a result of antagonistic interactions between fgf8 and bmp4 [20]. Analysis of pitx2 expression in s22 ta2 embryos shows expression in the frontonasal epidermis that correlates with the altered medial expression domains of fgf8 and bmp4 (Figures 3G and 3H). Importantly, pitx2 shows ectopic expression along the lateral aspect of the forming maxillary process and punctate foci of expression on the lateral maxillary process marking sites of tooth formation (arrows and arrowheads respectively, Figure 3H). Analysis of shh expression shows expression in the presumptive oral cavity (Figure 3I). In ta2, shh expression mirrors the changes seen in fgf8 and bmp4 expression boundaries, and it marks a reduced region of oral epidermis (Figure 3J). The coordinated change in expression of these genes at this early stage correlates with the formation of a novel oral/aboral boundary formed in the mutant as shown in anatomical and histological analyses (Figure 1). This is accompanied by early initiation of gene expression, consistent with the specification of toothforming regions in the mutant.

Developmental Potential of the Oral/Aboral Epidermis

As shown in recombination studies, the avian ectoderm and mesenchyme both have potential to participate in tooth development. Given the association of the observed outgrowths and the novel position of the oral/aboral boundary in the mutant, we postulated that initiation of tooth programs in the ta2 chick was due to the developmental repositioning of an epithelium with signaling potential to overlie mesenchyme competent to form teeth.

Constitutive activation of β-catenin in the epidermis has been shown to be sufficient to induce ectopic integumentary appendages during hair development in mice and feather formation in birds [29–31]. We used forced expression of an activated β-catenin [29] in the forming jaw as an epithelial signal to test the hypothesis that there is differential potential to form appendages in the oral versus aboral epidermis. Ectodermal expression of activated β-catenin (RCAS-β-catenin) resulted in the formation of tooth-like appendages in wild-type chickens (100%, n = 3; control, 0%, n = 3; Figures 4A–4J). The epidermal structures formed evaginated outgrowths that were histologically similar to those found in ta2 (Figures 4B–4D). These ectopic structures expressed shh in a punctate pattern, indicating that appendage developmental programs were initiated (Figures 4E–4J). We found that the majority of forced expression of activated β-catenin in the aboral epidermis, as measured by expression of the viral glycoprotein 3c2, was not sufficient to elicit shh expression or appendage growth (compare Figures 4E–4H with Figures 4K–4N). Thus, there is an intrinsic difference in developmental potential between the chick oral and aboral epidermis: Given expression of activated β-catenin, the chick oral epidermis is capable of making integumentary outgrowths whereas the aboral epidermis is not. Interestingly, when epithelium from the developing chick mandible is grafted to competent mesenchyme of feather-forming regions, new appendages are made only on the oral side of the graft (see Figure 4 of reference [8]); these outgrowths resemble the formations seen in the ta2 mutant.

Development and Evolution of Avian Teeth

Reports in the 19th century byG. St. Hillaire [32], followed by Blanchard [33] andGardiner [34], described the formation of transient papillae, initially argued as homologous to reptilian teeth, on the jaw of embryonic birds. These, however, were later discounted as similar to the dermal papillae seen in other integumentary structures, and the proposal was abandoned ([35], discussed in [34]). We show the initiation of tooth developmental programs as well as the formation of conical, saber-like structures on the lower jaw of the ta2 chicken. The structures formed are similar to those seen in the first-generation teeth of the alligator in position, histological differentiation, and morphogenesis. This finding is consistent with the idea that developmental programs are hierarchical and that atavisms will reinitiate early steps before later processes of more complex teeth. Previous reports interpreted tooth formation in light of knowledge of mammalian tooth development and thus searched for the elusive chick molar. Our work demonstrates a phylogenetic framework in which to interpret the latent ability of avian embryos to form teeth apart from mammalian tooth development.

We show that in ta2, the initiation of tooth developmental programs at a novel boundary formed as a result of altered specification of the oral/aboral junction early in development. We propose that this altered positioning of the oral/aboral boundary in the mutant leads to a juxtaposition of a presumptive boundary signaling center with underlying oral mesenchyme competent to form teeth (Figure 4O). The outgrowths in the mutant are patterned and show regional regulation of gene expression as well as specific differentiation, consistent with tooth formation in other vertebrates. Whether the matrix seen in both ta2 and alligator outgrowths is dentine awaits further biochemical and molecular analysis. Because grafting of the putative epithelial boundary region over competent mesenchyme leads to ta2-like tooth outgrowths in the oral region [8], we believe that the effect of the ta2 gene on tooth developmental programs is secondary, resulting from changes in the regional specification of a lateral tooth-inductive signaling center rather than specifically altering a molecular modifier of ontogenetic pathways.

We hypothesize that the loss of teeth in birds was due to the loss of direct apposition between an epithelial signaling center at the oral/aboral boundary and the underlying mesenchyme of the oral cavity competent to form integumentary appendages. Our model provides a unique developmental mechanism for understanding how specific structures are lost and reinitiated and goes beyond contemporary models of selective gene loss or loss of signaling capability during tooth ontogeny in evolution [2, 8]. Importantly, the control of this inductive event in different facial prominences during development would permit the regional, or modular, loss of teeth as seen in many nonavialan dinosaurs and avialans [4–6] while allowing them to retain the ability to form teeth on separate regions of the jaw derived from different facial prominences.

Our data support and revitalize the controversial anatomical findings of G. St. Hilaire [32], Blanchard [33], and Gardnier [34] by demonstrating the initiation of tooth developmental programs in embryonic birds, and we propose that the structures formed, and the early developmental processes involved, are homologous with the formation of the first rudimentary teeth in the alligators.

So if birds didn't have reptilian ancestors, how come the above researchers were able to reproduce the development of reptilian teeth in a modern bird mutant?

questioner121 wrote:As has been observed with the definition of the term "species" it is plastic in certain areas. The reason being that as new observations are made the interpretation of the evidence used to define species has found to be invalid.

Your duplicitous misuse of my expositions on this subject is duly noted. What was found to be invalid was the static view of species, arising from a misunderstanding of the difference between descriptive and prescriptive views of taxonomy.

questioner121 wrote:Just because there are no ring species around which have the complete successive chains leading from one species to an entirely different one due to extinctions or whatever else

Actually, you've been presented with examples of ring species that are alive. The lies you're posting here are becoming ever more desperate.

questioner121 wrote:does not in anyway justify or support common ancestry to the level of acceptance it has today.

Bullshit. We have multiple independent lines of evidence all pointing to the same conclusion. It's game over for mythology-based religious fantasies. Suck on it.

questioner121 wrote:As I said before you need to look more closely at why certain species cannot reproduce with one another rather than going by "incompatibility due to changes over time".

Oh wait, I've already told you to look up fertillin genes. Which, wait for it, acquire changes over time leading to those incompatibilities.