A single set of genes drives pufferfish spines, mouse hair, and chicken feathers

Brother Brian @2 >I agree. We have long known that scales, hair and feathers all have the same evolutionary origin. We don't know that; it is an evolutionary assumption with little evidence. Scales are a type of skin fold while hair and feathers are separate things that grow in the skin. They're quite different. aarceng

OLV, thanks for linking to the whole article and not just a summary. Interesting use of genetic research to propose an evolutionary tree. rhampton7

talking about puffer fish, this short video alone destroys evolutionary theory, unless you evolutionists believe, that this small fish took math lessons. make sure you watch the whole video https://www.youtube.com/watch?v=B91tozyQs9M martin_r

Evolution and Developmental Diversity of Skin Spines in Pufferfishes Takanori Shono, Alexandre P. Thiery,  Rory L. Cooper, Daisuke Kurokawa, Ralf Britz, Masataka Okabe, Gareth J. Fraser DOI: 10.1016/j.isci.2019.06.003 Article

Eda signaling may play a role in the evolutionary transition from spinoid scale to spine. Furthermore, shifts in expression of signaling pathways (such as Bmp) at various stages of appendage development have likely produced tremendous diversity in patterning and unit morphology in this group of derived teleost fishes. Future work on comparative expression patterns or transcriptome analyses may uncover a network of genes related to scale formation that can be directly compared with developing spines, potentially highlighting the genes lost or gained during the scale-to-spine transition.

OLV

I think what is being overlooked here is that there is no transitional form between scales and feathers. This is one of the “missing link” problems. In other words, we do NOT know that scales and feathers have the same evolutionary origin. Belfast

as to "How is this a problem?" Well besides the fact that the evolutionary origin of a single gene and/or protein is shown to be astronomically unlikely, much less have Darwinists ever empirically demonstrated the origin of a single gene and/or protein,,,

Yockey and a Calculator Versus Evolutionists - Cornelius Hunter PhD - September 25, 2015 Excerpt: In a 1977 paper published in the Journal of Theoretical Biology, Hubert Yockey used information theory to evaluate the likelihood of the evolution of a relatively simple protein.,,, Yockey found that the probability of evolution finding the cytochrome c protein sequence is about one in 10^64. That is a one followed by 64 zeros—an astronomically large number. He concluded in the peer-reviewed paper that the belief that proteins appeared spontaneously “is based on faith.” Indeed, Yockey’s early findings are in line with, though a bit more conservative than, later findings. A 1990 study of a small, simple protein found that 10^63 attempts would be required for evolution to find the protein. A 2004 study found that 10^64 to 10^77 attempts are required, and a 2006 study concluded that 10^70 attempts would be required. These requirements dwarf the resources evolution has at its disposal. Even evolutionists have had to admit that evolution could only have a maximum of 10^43 such experiments. It is important to understand how tiny this number is compared to 10^70. 10^43 is not more than half of 10^70. It is not even close to half. 10^43 is an astronomically tiny sliver of 10^70. Furthermore, the estimate of 10^43 is, itself, entirely unrealistic. For instance, it assumes the entire history of the Earth is available, rather than the limited time window that evolution actually would have had.,,, http://darwins-god.blogspot.com/2015/09/yockey-and-calculator-versus.html What is the maximum number of trials evolution could have performed? Kirk Durston - April 2016 Excerpt: Extreme upper limit for the total number of possible gene families sampled for all of life over 4 billion years = 2.2 x 10^45 trials. I have been extremely generous – by two orders of magnitude in comparison to a peer reviewed estimate for ‘an extreme upper limit’ of 4 x 10^43 trials (3). Since Dryden estimates 10^43 as his ‘extreme upper limit’, and it is peer reviewed, we will use his estimate instead of mine.,,, With 10^43 trials, one would think there would be no problem. Unfortunately, there are virtually no sequences that will produce stable, functional 3D structures. For example, RS7 is a universal protein required for all life forms, yet only 1 in 10^100 sequences will produce a functional RS7 protein domain. Obviously, in order for evolution to find any RS7 sequences, 10^43 trials is woefully inadequate – by 57 orders of magnitude. http://p2c.com/students/what-is-the-maximum-number-of-trials-evolution-could-have-performed/

Besides that little inconvenient fact, the alternative splicing patterns are found to be very different between different kinds of species. As the following article states, "A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,, " “the papers show that most alternative splicing events differ widely between even closely related species. The alternative splicing patterns are very different even between closely related species, i.e. humans and chimpanzees,”

Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012 Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,, A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species. On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,, http://www.the-scientist.com/?articles.view%2FarticleNo%2F33782%2Ftitle%2FEvolution-by-Splicing%2F

And yet, alternative splicing patterns are part of the Gene Regulatory Network:

Rethinking gene regulatory networks in light of alternative splicing, intrinsically disordered protein domains, and post-translational modifications - 2016 Abstract Models for genetic regulation and cell fate specification characteristically assume that gene regulatory networks (GRNs) are essentially deterministic and exhibit multiple stable states specifying alternative, but pre-figured cell fates. Mounting evidence shows, however, that most eukaryotic precursor RNAs undergo alternative splicing (AS) and that the majority of transcription factors contain intrinsically disordered protein (IDP) domains whose functionalities are context dependent as well as subject to post-translational modification (PTM). Consequently, many transcription factors do not have fixed cis-acting regulatory targets, and developmental determination by GRNs alone is untenable. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4341551/

But early acting mutations to Gene Regulatory Networks, (early acting mutations which are necessary to explain the supposed Darwinian origin of new body plans), are now shown to always be ''catastrophically bad"

A Listener's Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question - Casey Luskin - December 4, 2013 Excerpt: "There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way." - Eric Davidson - developmental biologist http://www.evolutionnews.org/2013/12/a_listeners_gui079811.html

Thus, where Darwinists most need plasticity in the genome to be viable as a theory, (i.e. developmental Gene Regulatory Networks), is the place where mutations are found to be almost 'always catastrophically bad'. Yet, it is exactly in this area of the genome (i.e. regulatory networks) where substantial, ‘orders of magnitude’, differences are found between even the supposedly closely related species of chimps and humans. Needless to say, since Darwinian evolution presupposes the unlimited plasticity of organisms, then the finding of inflexible, yet radically different, alternative splicing patterns, (developmental gene regulatory networks), between even supposedly closely related species is exactly the opposite finding for what would have been predicted to be found by Darwinists. If Darwinian evolution were a normal science that was subject to rigorous testing, instead of the pseudo-science that relies on an almost endless litany of 'just so stories' to cover up embarrassing empirical shortcomings, this finding, by itself, besides all the other falsifications of Darwin's theory, should have been more than enough to falsify neo-Darwinian claims.

Still Awaiting Engagement: A Reply to Robert Bishop on Darwin's Doubt - Paul Nelson - September 8, 2014 Excerpt: "Neo-Darwinian evolution is uniformitarian in that it assumes that all process works the same way, so that evolution of enzymes or flower colors can be used as current proxies for study of evolution of the body plan. It erroneously assumes that change in protein coding sequence is the basic cause of change in developmental program; and it erroneously assumes that evolutionary change in body plan morphology occurs by a continuous process. All of these assumptions are basically counterfactual. This cannot be surprising, since the neo-Darwinian synthesis from which these ideas stem was a pre-molecular biology concoction focused on population genetics and adaptation natural history, neither of which have any direct mechanistic import for the genomic regulatory systems that drive embryonic development of the body plan." Eric Davidson - 2011 ,, it is difficult to miss Davidson's thrust. As far as the origin of animal body plans is concerned, neo-Darwinism isn't incomplete or insufficient. It is dead wrong.,,, - per evolution news Stephen Meyer - Responding to Critics: Marshall, Part 2 (developmental Gene Regulatory Networks) - video https://www.youtube.com/watch?v=Cg8Mhn2EKvQ

Of related note, the overlapping coding of the genome, including the overlapping coding of Alternative splicing, is far more problematic to Darwinian presuppositions than they will ever openly admit in public:

Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing - 2016 In Brief Alternatively spliced isoforms of proteins exhibit strikingly different interaction profiles and thus, in the context of global interactome networks, appear to behave as if encoded by distinct genes rather than as minor variants of each other.,,, Page 806 excerpt: As many as 100,000 distinct isoform transcripts could be produced from the 20,000 human protein-coding genes (Pan et al., 2008), collectively leading to perhaps over a million distinct polypeptides obtained by post-translational modification of products of all possible transcript isoforms (Smith and Kelleher, 2013). http://iakouchevalab.ucsd.edu/publications/Yang_Cell_OMIM_2016.pdf Time to Redefine the Concept of a Gene? - Sept. 10, 2012 Excerpt: As detailed in my second post on alternative splicing, there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins! While the fact that a single gene can code for so many proteins is truly astounding, we didn’t really know how prevalent alternative splicing is. Are there only a few genes that participate in it, or do most genes engage in it? The ENCODE data presented in reference 2 indicates that at least 75% of all genes participate in alternative splicing. They also indicate that the number of different proteins each gene makes varies significantly, with most genes producing somewhere between 2 and 25. http://networkedblogs.com/BYdo8 Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - May 2013 Conclusions: Our analysis confirms mathematically what would seem intuitively obvious - multiple overlapping codes within the genome must radically change our expectations regarding the rate of beneficial mutations. As the number of overlapping codes increases, the rate of potential beneficial mutation decreases exponentially, quickly approaching zero. Therefore the new evidence for ubiquitous overlapping codes in higher genomes strongly indicates that beneficial mutations should be extremely rare. This evidence combined with increasing evidence that biological systems are highly optimized, and evidence that only relatively high-impact beneficial mutations can be effectively amplified by natural selection, lead us to conclude that mutations which are both selectable and unambiguously beneficial must be vanishingly rare. This conclusion raises serious questions. How might such vanishingly rare beneficial mutations ever be sufficient for genome building? How might genetic degeneration ever be averted, given the continuous accumulation of low impact deleterious mutations? http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006

bornagain77

rhampton7:

How is this a problem?

It isn't a problem for Intelligent Design as a Common Design explains it quite well. However evolution by means of blind and mindless processes could never produce such genes. ET

Brother Brian:

We have long known that scales, hair and feathers all have the same evolutionary origin.

Except for the fact no one has any such knowledge. No one knows how blind and mindless processes could have produced scales, hair and feathers. ET

R7

How is this a problem?

I agree. We have long known that scales, hair and feathers all have the same evolutionary origin. Brother Brian

How is this a problem? rhampton7