Well's may have done a PhD in developmental biology but I think it is generous to still call him a developmental biologist. He had 2 publications from his PhD research in 1996 and 97 and has only published one thing since, a purely speculative paper about a role for polar ejection forces generated by centrioles in causing cancer which was published in 2005. So it is over a decade since Well's had any published research in the field of developmental biology.
"When an egg's genes are removed and replaced by those of another type of animal, development follows the pattern of the original egg until the embryo dies from the lack of the right proteins"
Well's is essentially correct here. There are certainly exceptions amongst closely related species, such as the many ongoing experiments to regenerate extinct or threatened species by SCNT into related species, but most highly divergent species will not develop to term in such a case. I certainly don't think that the cat-rabbit experiments you discussed gave rise to full term cat clones.
This is because the oocyte is nothing like identical in many different species. If you compare a human oocyte to a Xenopus you will find they are 1/10th the size and of strikingly different composition with the Xenopus oocyte containing large quantities of yolk proteins for the embryo to feed on.
"Biologists have found that mutations in developmental genes often lead to death or deformity, but they never produce changes that benefit the organism..."
Well this is a disingenuous argument. By far the vast majority of mutational experiments in developmental biology are done with the explicit purpose of breaking genes to such an extent that they cause death or deformity. This is done because death and deformity are nice readily apparent things which can be easily identified and scored. So most mutational studies are crudely designed to make large severe damaging mutations with ionising radiation or potent mutagenic chemicals.
These experiments are done to elucidate the normal course of devlopment, that is why they are developmental biology experiments. When it comes to looking for beneficial mutations in an experimental setting evolutionary biologists will normally tend to look at microorganisms with generation times measured in hours or days rather than multicellular organisms with generation times in weeks or months.
The only way to identify beneficial mutations is by following the success of various mutations in a population and observing which ones confer improved reproductive success. Obviously this takes several generations to properly establish as you need to exclude the effect of random factors causing genetic drift.
So Well's is technically correct that this hasn't been seen experimentally but neglects to mention that no one is actually doing such experiments to generate beneficial mutations in specifically developmental genes. He assumes such mutations do not exist, but he has no evidence for it. There are examples of beneficial mutations in a number of other types of genes such as metabolic genes allowing for insecticide resistance.
"DNA mutations never alter the endpoint of embryonic development: they can't even change the species"
Clearly this argument is confused, the various deformities Well's previously mentioned are examples of DNA mutations altering the developmental endpoint. If he means thta we don't see frogs giving birth to cats, well that is evolution as only a creationist could understand it.
He is certainly wrong about changes in DNA not giving rise to new species, although as a creationist his definition of species may be highly idiosyncratic. There are numerous examples from Drosophila of cases where the genetic basis of reproductive isolation, arguably an efffective definiton of distinct species, has been clearly identified.
Anopther such paper on the same species is (Brideau et al., 2006) which is interesting as it again describes hybrid incompatibility between D. simulans and D. melanogaster. In fact the experiments done in the Nup160/Nup96 papers were performed on hybrids which had had the incompatibility caused by the appropriately named Lethal hybrid rescue gene rescued, protecting the hybrid males from their usual fate of death.
So these experiments identified 4 distinct genes with specific mutations combinations of which could produce reproductive isolation but which indivdually did not, therefore allowing the existence of hybrid populations as intermediates between the two distinct species.
He goes on about microtubule arrays and membrane patterns in the egg, and how those arrays are created by mysterious organelles called centrosomes which are inherited independently of an organism's DNA.
Why does he think these are mysterious? This is one of those words like complex which creationists think will magically make their argument for them despite being completely worthless in scientifc terms. Membranes aren't produced by centrosomes, I think either you or Well's misunderstood something. Or does membrane patterns refer to membrane associated feature like the cilia or transmembrane proteins?
In any case as Mr. Jack points out it is incorrent to say these are independent of DNA. They are not all synthesised de novo in the new zygote after fertilisation but they were dependent on a number of proteins coded by DNA for their creation. Obviously this is an example of 'irreducible complexity' in the trivial sense that without one element the other could not exist in its current state, it is considerably harder to show that it is 'irrecudibly complex' in the sense that such a system could not evolve from functional intermediates, indeed cell division in the absence of a centrosome has been shown to occur and indeed the full development of adult flies (Megraw et al., 2001).
Basically he's bringing this up to show that this can't be explained by our current theory of evolution.
This may be why, but it doesn't do that. It certainly shows that DNA is not the be all and end all of development, or evolution, but then no develop mental biologist has held that view for about the last 30 years. Epigenetic factors are readily accepted as a key component in development, indeed one of the major problems with intraspecies, let alone cross species, SCNT is the presence of epigenetic markers which make the DNA distinct from that in a newly fertilised zygote.
If you can't get from one species of animal to another by replacing or mutating its DNA, then the Darwinian explanation is finished.
This seems reasonable, but it also happens to be demonstrable that you can do this in some cases, i.e. the Drosophila species I mentioned previously.
Also, since all cells have the same DNA, and yet cells differentiate themselves into different types during development, something outside of the cell's DNA has to be in play
Absolutely, but in a lot of cases it is simply the products of that cells DNA. The whole way development produces thgese different cell types is not through magical effects of mysterious organelles like the centrosome but through the complex interaction of the whole embryonic environment with the genome.
To act as if this is all a complete mystery is simply to ignore all of the devlopmental research of the last 30-40 years which has been an ongoing process elucidating exactly how differentiation and diversification occur.
I gather that the morphology of this egg development is not monitored by genes. Have I understood it correctly?
This depends on exactly what you mean. I think 'monitored' is the wrong term, the genes rather direct the development. Whose genes do this is the key fact here however. In cases like the Xenopus and Drosophila oocytes there are many proteins which are deposited in the egg by the mother, and these proteins affect the subsequent development of the embryo through its earliest stages. For this reason some oocytes, such as those of Xenopus can be mechanically stimulated to begin undergoing the first few cleavage stages even if the genetic material has been removed.
Could this association and specialization have also nothing to do with genes? What is your opinion?
I'd say almost certainly not. Although I'm not aware of any specific research into the genetic basis of coloniality/multicellularity in the Volvocales, which are perhaps the most commonly studied multicellular algal forms. I know that Chlamydomonas is often put forward as a model for the unicellular precursor of colonial algae.
Maybe I miss some important point, but, if original genes are removed and replaced by those of another species, and development follows the pattern of original species, how can genes have directed this?
There are a few possible outcomes in development of a SCNT embryo: In one the replacement DNA is from a species closely related enough that it produces a viable embryo, in which cases the eary embryonic stages are likely to be very similar anyway, for instance SCNT between llamas and camels can produce a viable embryo that will develop into a hybrid.
Another posibility is that, as Wells has been quoted saying in this thread, the genome are incompatible and the embryo dies at an early developmental stage, often after only one or two cell divisions. In certain animals, such as amphibians and insects, maternally deposited proteins and gene transcripts control the embryo for several stages of early development until what is called the mid-blastula transition (MBT), when the embryos own zygotic genes take over. Obviously in such embryos the compatibility of the genome is not relevant until the MBT.
So in some species the genes directing embryonic development until the MBT are those of the mother which deposited the proteins and mRNA in the oocyte.
Edited by Wounded King, : No reason given.
Edited by Wounded King, : Sorry, I messed up the camel/llama example, it isn't actually SCNT at all, just cross species breeding, I should have gone back and checked the literature.
According to him, if the developmental plan is not fully specified by the DNA, then mutations to DNA are not enough to produce a new type of animal (or species)
This is clearly not the case. Even if the developmental plan is not fully specified by DNA it doesn't follow that changes in DNA are insufficient to produce a new species or sufficient morphological change to constitute a new type of animal. All it would need surely is for the body plan to be substantially specified by the DNA. We know that environmental factors can effect the development of a growing embryo, but we also know that genetic factors can effect embryonic development. One does not preclude the other.
I don't think that's what Wells is talking about.
That is because Wells is constructing a strawman which has little if any relevance to evolution. Evolution does not proceed by a whole human genome suddenly appearing as if by magic in a chimpanzee oocyte. Both the oocyte composition and the genome are changing over the same period of evolution.
If you don't get a human with an entire set of human DNA, then there must be more that's needed.
We've already answered this half a dozen times. The oocytes of different species are different. The composition of those oocytes is not produced by the genetic complement of the embryos, it is rather a product of the maternal DNA. Not everything needed for development is provided by the Oocyte/embryonic DNA, after all at some stage it will need input from its external environment even if it is just gaseous/oxygen exchange. In general the more closely related species are the more likely a nuclear transfer is to succeed in developing to later stages.
It is important to bear in mind that the common technique of Somatic cell nuclear transfer has added barriers in many organisms due to the accumulation of epigenetic modifications to the genome. These modifications such as DNA methylation and histone methylation and acetylation change the dynamics of expression of various genes in the somatic cell and can lead to incompatibilities of the somatic nuclear DNA with the host oocyte, this occurs even in the same species and is why Dolly as a successful example of mammalian SCNT was such a breakthrough.
One good example of an at least partially independent organelle is the mitochondrion, I imagine that Wells prefers cytoplasmic structures and microtubules though since the mitochondrion actually has its own genetic complement, blowing a further hole in Wells's attempts to marginalise the role of DNA. It is worth noting though that the mitochondrion still requires gentic elements in the host cell nuclear genome to function properly and replicate. Except for a handful of cases inheritance of mitochondria is exclusively maternal, another example of the maternal genome determining the composition of the Oocyte, and extended genome included the mitochondrial DNA in this case.
But DNA doesn't hold "shape data" does it?
Not as an interpretable set of 3D coordinates no, but it arguably contains the network of procedural rules for generating the correct 3D structure.
Where exactly is the "3D geometry data" that defines for example, the shape of your skull, located? If cells need to differentiate themselves into structures like that, where is that specified?
This question is of course the entire focus of developmental biology and it is not one that has been fully answered. But as far as we have one the answer is very clearly that the shape is indeed specified by the genome, though obviously it is not stored as any form of "3D geometry data", rather it is stored in a complex network of interacting proteins and enzymes coded for by DNA and the multiple non-coding genetic elements with which they interact. This is clearly seen in the fact that changes in DNA can lead to changes in the skull morphology, exactly the sort of change in developmental endpoint that Well's denies exists. One example of this, not the skull per se, is in the effect of Bone Morphogenetic Protein on the shape of avian beaks (Wu et al., 2006). For a review of elements of cranial skull development and some of what we know about its genetic basis see Opperman (2000).
Sounds like membrane patterns and microtubule arrays according to Wells.
There is absolutely not a scrap of evidence for this, and I'm not even sure Wells goes as far as to make such a specific claim does he?
On another forum I asked for a Darwinian explanation for an observation made by Alfred Wallace which ended up that way, and no Darwinian explanation was provided, nor would it be expected that anybody ever could, because it's a failure of a theory to account for all relevant things.
Maybe you should pose the same conundrum to us in another thread.
I think that this post addresses some of the same issues as were raised in Ganondorf's new topic proposal.
The only specifc example that Dr. Zaid gives on his website as evidence that DNA does not contribute to shape is that he says the deposition of collagen is not controlled by DNA once it has left the cell, and therefore the shape of a developing hand, is largely due to the deposition of collagen as extracellular matrix.
Dr. Zaid writes:
To know the answer to this question we need to understand how genes and DNA work, the genes are part of the information contained in the DNA molecule such that this information when it is read it becomes a protein and proteins are the building blocks of living creatures (like the bricks, glass, and stone comprising a building). The DNA is found only in the nucleus of the cell and as such the controlling action of the DNA is localized within the cell (shown in figure (2) part (A)).
So when the proteins leave the cell (taking the collagen protein as an example) and they are found in the space outside of the cell (shown in figure (2) part (B)), then the big question now is: Can the DNA control the collagen proteins to form the shape of the hand for example (shown in figure (2) part (C))?
The answer is NO, because as we said the control of the DNA is found only within the nucleus of the cell. Thus it can be concluded that genes and DNA can not code (memorize) the design information of a creature and as such design changes occurring in a certain generation of organisms can not be transferred to the next generation using genes and so there is no basis for the evolution claim.
His argument really doesn't make any sense. While DNA may not actively direct the transport of collagen once it has left the cell the distribution of collagen producing cells is governed by different levels of gene expression in response to specific morphogenic signals which are themselves the protein products of DNA.
Apparently Dr. Zaid has never bothered to study anything in the field of developmental biology.