Dr. Stephen Meyer and Dr. Douglas Axe were recently interviewed by author and radio host Frank Turek on the significance of November’s Royal Society Meeting on evolution, in London. The two Intelligent Design advocates discussed what they see as the top five problems for evolutionary theory:
(i) gaps in the fossil record (in particular, the Cambrian explosion);
(ii) the lack of a naturalistic explanation for the origin of biological information;
(iii) the necessity of early mutations during embryonic development (which are invariably either defective or lethal) in order to generate new animal body types;
(iv) the existence of non-DNA epigenetic information controlling development (which means that you can’t evolve new animal body plans simply by mutating DNA); and
(v) the universal design intuition that we all share: functional coherence makes accidental invention fantastically improbable and hence physically impossible.
In today’s post, I’d like to focus on the third argument, which I consider to be the best of the bunch. The others are far less compelling.
Over at the Sandwalk blog, Professor Larry Moran and his readers have done a pretty good job of rebutting most of these arguments, in their comments on Professor Moran’s recent post, The dynamic duo tell us about five problems with evolution (January 14, 2017). Larry Moran’s earlier 2015 post, Molecular evidence supports the evolution of the major animal phyla cites a paper by Mario dos Reis et al. in Current Biology (Volume 25, Issue 22, p2939–2950, 16 November 2015) titled, “Uncertainty in the Timing of Origin of Animals and the Limits of Precision in Molecular Timescales,” which convincingly rebuts Meyer and Axe’s first argument, by showing that animals probably originated in the Cryogenian period (720 to 635 million years ago) and diversified into various phyla during the Ediacaran period (635 to 542 million years ago), before the Cambrian. I might add that we now have strong evidence that anatomical and genetic evolution occurred five times faster during the early Cambrian, at least for arthropods – although as Intelligent Design advocates have pointed out, that still leaves unanswered the question of how animal body plans arose in the first place.
Meyer and Axe’s second argument asserts that natural processes are incapable (as far as we can tell) of creating significant quantities of biological information – and especially, new functions or new anatomical features. Much of the argument rests on the alleged rarity of functional proteins in amino acid sequence space – a claim that was crushingly refuted in Rumraket’s recent post on The Skeptical Zone titled, Axe, EN&W and protein sequence space (again, again, again) (October 12, 2016). As for the claim that natural processes can’t create new functions, it’s simply bogus. The following three papers should be sufficient to demonstrate its empirical falsity: Five classic examples of gene evolution by Michael Page (New Scientist Daily News, March 24, 2009), Evolution of colour vision in vertebrates by James K. Bowmaker (Eye (1998) 12, 541-547), and Adaptive evolution of complex innovations through stepwise metabolic niche expansion by Balazs Szappanos et al (Nature Communications 7, article number 11607 (2016), doi:10.1038/ncomms11607).
I’m not really qualified to discuss Meyer and Axe’s fourth argument, but it seems to me that Professor Larry Moran has addressed it more than adequately in his recent post, What the Heck is Epigenetics? (Sandwalk, January 7, 2017). The last four paragraphs are worth quoting (emphases mine):
The Dean and Maggert definition [of epigenetics] focuses attention on modification of DNA (e.g. methylation) and modification of histones (chromatin) that are passed from one cell to two daughter cells. That’s where the action is in terms of the debate over the importance of epigenetics.
Methylation is trivial. Following semi-conservative DNA replication the new DNA strand will be hemi-methylated because the old strand will still have a methyl group but the newly synthesized strand will not. Hemi-methylated sites are the substrates for methylases so the site will be rapidly converted to a fully methylated site. This phenomenon was fully characterized almost 40 years ago [Restriction, Modification, and Epigenetics]. There’s no mystery about the inheritance of DNA modifications and no threat to evolutionary theory.
Histone modifications are never inherited through sperm because the chromatin is restructured during spermatogenesis. Modifications that are present in the oocyte can be passed down to the egg cell because some of the histones remain bound to DNA and pass from cell to cell during mitosis/meiosis. The only difference between this and inheritance of lac repressors is that the histones remain bound to the DNA at specific sites while the repressor molecules are released during DNA replication and re-bind to the lac operator in the daughter cells [Repression of the lac Operon].
Some people think this overthrows modern evolutionary theory.
So much for epigenetics, then.
The fifth and final argument discussed by Drs. Meyer and Axe relates to the universal design intuition. I’ve already amply covered both the merits and the mathematical and scientific flaws in Dr. Axe’s book, Undeniable, in my comprehensive review, so I won’t repeat myself here.
The “early embryo” argument, helpfully summarized by Dr. Paul Nelson
That leaves us with the third argument. Looking through the comments on Professor Moran’s latest post, it seems that very few readers bothered to address this argument. The only notable exception was lutesuite, who pointed out that examples of non-lethal mutation in regulatory DNA sequences are discussed in a paper titled, Functional analysis of eve stripe 2 enhancer evolution in Drosophila: rules governing conservation and change by M.Z. Ludwig et al. (Development 1998 125: 949-958). The paper looks interesting, but it’s clearly written for a specialist audience, and I don’t feel qualified to comment on it.
As it turns out, I wrote about the “early embryo” argument in a 2012 post, when it was being put forward by Dr. Paul Nelson. Nelson handily summarized the argument in a comment he made over at Professor Jerry Coyne’s Website, Why Evolution Is True:
Mutations that disrupt body plan formation are inevitably deleterious. (There’s only one class of exceptions; see below.) This is the main signal emerging from over 100 years of mutagenesis in Drosophila.
Text from one of my Saddleback slides:
1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows.
2. Thus, to change — that is, to evolve — any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring.
3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo.
Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes.
Obviously, loss of function is incapable of explaining the origin of new, viable body plans for animals.
A hole in the argument?
On the face of it, Nelson’s three-step argument certainly looks like a knock-down argument, assuming that the premises are factually true. But are they? A commenter named Born Right made the following response to Dr. Nelson over at Jerry Coyne’s Website (emphases mine):
Paul Nelson,
Lethal mutations will kill the embryo. But what you’re totally failing to understand is that not all mutations are lethal. Many are tolerated. I heard you cite the example of HOX gene mutations in flies and how altering them kills the embryos. You didn’t mention the entire story there. Do you know that there are wild populations of flies having HOX gene mutations? Even in the lab, you can create viable HOX-mutant flies that have, for example, two sets of wings. In fact, simple non-lethal mutations in HOX genes can profoundly alter the morphology. It is these non-lethal mutations that natural selection “cherry picks”, provided they confer a survival advantage on the organism.
Many mutations actually arise as recessive mutations, not as dominant ones. They spread through the population remaining dormant or having a mild effect, until there is a sufficient number of heterozygotes. Then, interbreeding between heterozygotes will cause homozygous mutations to arise suddenly throughout the population. If the new feature improves survival & reproductive success, it gets rapidly selected…
Macroevolution is a gradual response to climate change and other environmental pressures. Organisms accumulate non-lethal mutations that changes their body plan bit by bit until they are well adapted to their changing habitat.
However, a 2010 Evolution News and Views post co-authored by Dr. Paul Nelson, Dr. Stephen Meyer, Dr. Rick Sternberg and Dr. Jonathan Wells, contests the claim that Hox gene mutations are non-lethal. The authors assert that such mutations are, at the very least, defective:
Mutations to “genetic switches” involved in body plan formation … disrupt the normal development of animals. With the possible exception of the loss of structures (not a promising avenue for novelty-building evolution, in any case), these mutations either destroy the embryo in which they occur or render it gravely unfit as an adult. What the mutations do not provide are “many different variations in body plans.”…
… [T]here are solid empirical grounds for arguing that changes in DNA alone cannot produce new organs or body plans. A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12
None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
Indeed, the evidence justifies only one conclusion, which Wells summarized in his last slide at SMU:
“We can modify the DNA of a fruit fly embryo in any way we want, and there are only three possible outcomes:
A normal fruit fly;
A defective fruit fly; or
A dead fruit fly.”
The Wikipedia article on Drosophila embryogenesis may interest some readers.
What I would like to know is: are the Hox mutations in fruitflies mentioned by Born Right in his comment above neutral or deleterious – and if the latter, are they only slightly deleterious or highly deleterious?
A follow-up comment by Born Right
In a subsequent comment over at Why Evolution Is True, Born Right cited two scientific references in support of his claims:
Paul Nelson,
Fantastic new research shows how fish developed limbs and moved onto land. Boosting the expression of Hoxd13a gene in zebrafish transforms their fins into limb-like structures that develop more cartilage tissue and less fin tissue!
http://www.sciencedaily.com/releases/2012/12/121210124521.htm
http://www.sciencedirect.com/science/article/pii/S1534580712004789
Importantly, the overexpression of Hoxd13a in zebrafish was driven by a mouse-specific enhancer. This shows that the regulatory elements acting on the enhancer are present in both fishes and distantly-related mammals!
The first paper, titled, From fish to human: Research reveals how fins became legs (Science Daily, December 10, 2012) is written in a style that laypeople can readily understand. I’ll quote a brief excerpt (emphases mine):
In order to understand how fins may have evolved into limbs, researchers led by Dr. Gómez-Skarmeta and his colleague Dr. Fernando Casares at the same institute introduced extra Hoxd13, a gene known to play a role in distinguishing body parts, at the tip of a zebrafish embryo’s fin. Surprisingly, this led to the generation of new cartilage tissue and the reduction of fin tissue — changes that strikingly recapitulate key aspects of land-animal limb development. The researchers wondered whether novel Hoxd13 control elements may have increased Hoxd13 gene expression in the past to cause similar effects during limb evolution. They turned to a DNA control element that is known to regulate the activation of Hoxd13 in mouse embryonic limbs and that is absent in fish.
“We found that in the zebrafish, the mouse Hoxd13 control element was capable of driving gene expression in the distal fin rudiment. This result indicates that molecular machinery capable of activating this control element was also present in the last common ancestor of finned and legged animals and is proven by its remnants in zebrafish,” says Dr. Casares.
This sounds fascinating, and to me it constitutes powerful evidence for common ancestry, but the real question we need to address is; exactly how early in the course of the zebrafish’s embryonic development did these mutations take effect?
The second paper cited by Born Right (“Hoxd13 Contribution to the Evolution of Vertebrate Appendages” by Renata Freitas et al. in Developmental Cell, Volume 23, Issue 6, pp. 1219–1229, 11 December 2012) is much meatier, because it’s the original papaer on which the Science Daily report was based. The authors contend that “modulation of 5′ Hoxd transcription, through the addition of novel enhancer elements to its regulatory machinery, was a key evolutionary mechanism for the distal elaboration of vertebrate appendages,” and they conclude:
Within the developmental constraints imposed by a highly derived teleost fin, our results suggest that modulation of Hoxd13 results in downstream developmental changes expected to have happened during fin evolution. This, together with the evidence we provide that the upstream regulators of CsC were also present prior to tetrapod radiation, makes us favor an evolutionary scenario in which gain of extra 5′ Hoxd enhancers might have allowed the developmental changes necessary for the elaboration of distal bones in fishes that evolved, ultimately, into the tetrapod hand.
This sounds a lot more promising, but after having a look at it, I’m still rather unclear about exactly how early these hypothesized mutations would have had to have occurred, in the course of vertebrate embryonic development. Perhaps some reader can enlighten me.
Well, that’s about as far as my digging and delving has taken me. I’d like to throw the discussion open at this point. Are there any known examples of early embryonic mutations which are not deleterious, and do they shed any light on how new animal body plans might have evolved? Over to you.
(Note: the image at the top [courtesy of Wikipedia] shows the ventral view of repeating denticle bands on the cuticle of a 22-hour-old Drosophila embryo. The head is on the left.)
Frankie,
No it isn’t. The evidence is that a zygote produces proteins (rooted in DNA) and RNAs (ditto) which between them determine the developmental unrolling.
All proferred examples of ‘non-DNA’ factors so far have been from people who (like you) can’t think more than one step back, to how the molecule in question got there. Which is: ultimately from DNA, of this or a parent cell, via a causal chain.
[snip yet another argument-by-glove-puppet from someone who ‘agrees with Frankie’, as if there are no other experts in the world who take a contrary view].
That doesn’t determine the form, Allan.
I asked you to post any views to the contrary and you have failed. I have asked you to support you claim and you have failed.
The contention seems to be ‘if DNA is the source of all things, it ought to be possible to read the program off it’. I don’t see how that follows. It would be hard enough with actual programs – beyond a certain level of complexity, it becomes almost impossible to tell what will happen, especially if you only have the code in binary. With molecular systems, it’s harder still. ‘Produce this molecule for 15 days, then stop’ isn’t an instruction anywhere.
The mechanism are often activated by DNA, but we don’t know where the information for patterns for each cell type, cell phase, in the tissue type in the developmental phase reside.
I’ve already provided examples of experiments showing lots of heritable (not necessarily mutatable) information resides outside the DNA, the information for chromatin modifications could reside outside of the DNA, the alternative is to pack it inside the DNA the way 82.5 Megabytes Moran would suggest.
Below is a picture of methylation patterns between normal and cancerous cells. The yellow dots indicate methylation cites where there is no difference between normal and cancerous cells. The red dot indicates the change in methylation pattern in a cancer cell. It is from here:
https://www.spandidos-publications.com/article_images/ol/1/5/OL-01-05-0815-g00.jpg
Btw, this is similar to the work ENCODE does, which Graur and Moran are so quick to criticize.
So, the point is, we have different methylation patterns for different cell types, and when they are deviated from, it can result in disease. You say those patterns are in the DNA, but you provide no map for how DNA codes the methylation patterns. That’s probably because DNA doesn’t code the methylation patterns anymore than it codes the glycan patterns or the structural patterns in organelles or the histone code as 82.5 Megabytes Moran would have the world believe.
dazz
Thank you for your comments. Re de novo genes, let me say up-front that I agree with your claim that there are no genes without an homologous counterpart in some other species. I’ve written about this before, in the following posts on Uncommon Descent:
Human and chimp DNA: They really are about 98% similar
Double debunking: Glenn Williamson on human-chimp DNA similarity and genes unique to human beings
You also write:
First, I think the hypothesis of (intelligently designed) wild saltations definitely deserves to be taken seriously, as an explanation for the origin of animal body plans. Currently we don’t know enough to rule it out, however uncongenial it may sound to some.
I should also mention that in an article entitled, “Mobile DNA and evolution in the 21st century” (Mobile DNA 2010, 1:4 doi:10.1186/1759-8753-1-4, published 25 January 2010), Professor James Shapiro maintains that vertebrates and flowering plants appeared within a single generation, as a result of whole genome doubling [WGD], a mechanism which he describes as follows: “WGD is yet another evolutionary process outside the Darwinist perspective that occurs suddenly (that is, within a single generation) and simultaneously affects multiple phenotypic characters.” OK, that’s not intelligent design, but it’s a pretty sudden change. Shapiro seems to believe that animal body plans originated fairly suddenly, too.
You maintain that “[i]f all mutations in the genes that control animals’ body plan are deleterious, body plans can’t evolve, with or without ‘guidance.'” Well, That depends on how you define “mutation.” If it means any genetic change, then your conclusion does indeed follow (unless one were to posit that animals’ body plans are controlled by non-genetic factors, and that’s not a line I’m defending here). But if the genetic changes required to make a viable new body plan turned out to be multiple and had to be very carefully synchronized, then one might reasonably conclude that unguided processes could not have brought about these changes. Now, I don’t know if this is the case. But it might well be.
Finally, I do not claim that mutations can only reduce functionality. I argued to the contrary, in my review of Dr. Axe’s book, in which I supplied actual examples of mutations creating new functions.
Because the order happens to follow evolutionary patterns? Because the limitations are evolutionary ones?
Oh, that’s right, you don’t pay attention to the evidence, you just note the complexity and bleat “God did it.” Because you’re not out to explain anything at all, and your non-explanation is “God.”
Glen Davidson
stcordova,
But you’re talking about somatic cell lines again. Epigenetics, as John has already pointed out, is pretty much how tissues differentiate. And, as I have pointed out, methylation and demethylation tend to be mediated by (DNA-sourced) enzymes. Different ones are expressed in different tissues, and results are dependent both upon source and substrate, and the local cellular environment.
But this is not some massive paradigm shift, a Challenge to 21st Century Biology, The Death Of Darwin, or nuthin’.
Show us the scientific ToE that predicts tese patterns
Alan Miller,
I think the following comment of yours gets straight to the point:
That said, it doesn’t follow from the fact that all heritable information is rooted in DNA that it is reducible to DNA. There might be additional information in the cytoplasm that works in tandem with DNA.
I’d now like to turn to Sal’s suggestions regarding inheritance:
I take it Sal is not denying a role for DNA; he just thinks it isn’t the whole story. Is he right?
Back in 2014, there was an Uncommon Descent post titled, Jonathan Wells: Far from being all-powerful, DNA does not wholly determine biological form. The key word here is “wholly.” If that’s all that Dr. Wells wants to argue, then I’d say he’s probably correct. But he also writes in his book, The Myth of Junk DNA:
Wells cited the following paper in support of his claims: Gabius H-J (2000) Biological information transfer beyond the genetic code: The sugar code. Naturwissenschaften 87:108-121. doi:10.1007/s001140050687
A commenter named AVS responded (emphases mine):
Another commenter named Dr. JDD, who seems to be a specialist in this field, replied (emphasis mine):
Dr. JDD added:
I wonder if you (or Sal) would like to comment on Dr. JDD’s views.
Hi Sal,
In response to my question about how much source code you think is required to code for a human being, you write:
There are something like 10^15 connections in the human brain, but I see no reason to believe that each requires its own separate byte to code for it. The notion that 82.5 megabytes might be sufficient to store all the information required to make a human being sounds incredible, but sometimes incredible-sounding things turn out to be true.
Speaking of the human brain, I just came across a Live Science article saying that the human brain’s memory could store the entire Internet. Amazing. Cheers.
vjtorley,
That the story starts with DNA does not of course mean that it stops with DNA. Clearly, DNA exerts what influence it has firstly through its products. These products come up against an environment – an environment both externally and internally generated. That environment acts reflexively upon the genes – there is feedback, at several levels.
What a gene, or any protein or biochemically produced small molecule does – or whether it exists at all in a given cell – depends evidently on context, and that context is not ‘encoded’ to the nth degree in DNA itself. There is a causal cascade, but (IMO) DNA lies at its heart.
Still, what I perceive in these general exchanges is too much depth and not enough grasp of the basics. The ability to pontificate on cutting-edge research without apparently grasping some important biological distinctions is a problem with many commenters.
I’ll read ‘Dr JDD’ in more depth later, thanks.
vjtorley,
from wiki:History of orphan genes[edit]
VJT Do you disagree with this?
Frankie writes:
That’s actually quite a profound question. I would answer that the differences between living creatures also constitute a powerful part of the case for evolution. The most telling point is that the vast majority of these differences are known to be the result of neutral mutations, which can be observed in Nature all the time. What that means is that if intelligent guidance of evolution is going on, it pertains at most to a tiny (but significant) minority of the changes occurring in our genomes. As for the other differences, it seems that most of them can be selected for. Mutations that generate new body plans are a very rare occurrence.
In his book, Why Evolution Is True, Professor Jerry Coyne breaks the theory of evolution down into six notions: evolution (i.e. genetic change over time), gradualism, speciation, common ancestry, natural selection, and nonselective mechanisms of evolutionary change. You can find a brief but helpful discussion of these issues here.
Yes, I remember those, thanks
Wow, I don’t know what to say. Do you seriously think that it’s more plausible that entire body plans appeared in a single generation than gradually, in a step-wise manner?
How can you believe that a single tiny mutation of a certain type MUST be lethal, but somehow an invertebrate giving birth to a vertebrate is fine with you? Don’t you think that poses a MUCH bigger problem in terms of viability?
I’ll take a look at Shapiro’s paper later today, but I just can’t fathom how can one possibly argue for such an outrageous hypothesis, involving whole genome duplications to produce vastly different descendants, while quibbling about simple mutations. I believe yeast has undergone WGD, yet no visible new body-plan change ensued. Not affirming the consequent, but I wonder if there’s evidence of some correlation between WGDs and body plans, or evidence to the contrary.
It doesn’t really matter how one calls it, mutation or whatever. According to Paul Nelson changes in genes that affect early development are lethal. We know those changes happened because the genes are different in species and they share a common ancestor. Remember it’s Nelson who claims that those genes MUST have been altered to produce new body plans, it doesn’t matter if there are some other esoteric, non-genetic processes at play, Nelson claims that those genes must change, it’s a necessary precondition, whether it’s sufficient or not is completely irrelevant.
Again, how could such a process be viable at all? Reproductive processes are not just poof, there’s your descendants.
I know Vincent, I know. I’m addressing Nelson argument, and asking our local IDists to explore the consequences of accepting it. I appreciate your insight and your honesty.
Seems to me IDists often go with these arguments without exploring the entailments
vjtorley,
While searching for the Mandelbrot video I posted earlier I came across a nice Nova programme about fractals, and their role in biology. If construction can be fractal (and it appears that branching lineages of cells lend themselves quite well to this) then there can be an enormous amount of compression – complexity from simple rules.
Most of the genome is actually involved in cell maintenance rather than gross development. It takes quite a lot just to keep a nematode going! I think computing metaphors – and intuition – can be misleading.
Hi colewd,
The Wikipedia article also states: “Genes can be tentatively classified as orphans if no orthologous proteins can be found in nearby species.” This definition says nothing about the existence of non-coding homologues in nearby species. That was what my two UD articles were about (see comment #3 on this page).
Maybe we can run a few BLAST runs for those HOX genes. If we find some differences in closely related species, what do we make of Nelson’s argument?
First off, I should mention, it is very very early in the game as far as what we know. Larry and others in his camp portray human complexity as pretty much figured out in the 82.5 megabytes of the genome he thinks is functional (the rest being junk in his mind). This is premature and presumptuous. We know so very very little of what could be known. ID proponents in the IT industry are quick to point out that the Windows 10 operating system that requires 16 Gigabytes need almost 200 times more capacity than what Larry said is required to make something as complex as a human. Humans make Windows 10, not the other way around. At a gut level, the thought that 82.5 Megabytes to make something as complex as a human just seems absurd to many IT professionals with ID sympathies. That intuition is hard to suppress, hence I’m happy to keep quoting the 82.5 Mb figure since the absurdity of the that small figure resonates with many in the ID community.
I pointed to experiments that prima facie show that DNA does not provide the assembly instructions for how proteins coded by DNA connect to each other to make mitochondria or cilia, and that at the very least many organelles can be assembled from templates of pre-existing organelles much like a 3D copying operation, hence the DNA is only a necessary, but not sufficient part of the information description of structure.
Agree, the sugar code has a degree of independence from the genome. This should not be surprising in as much as I showed (with the cilia microsurgically modified) organelle structures have structural information not in the DNA.
But from Phys.org
The problem is we don’t have sequencing technology for the sugar code yet. The issue can be resolved in principle, hence I say it is early in the game. At best Larry is being way too premature, at worst he’s wrong. I say, let’s not rush to judgement on these matters.
Agree. I got the same impression from researches at the NIH who specialize in membrane trafficiing and transport. Perhaps a picture will help to visualize what Dr. JDD is talking about.
Below is a picture of heparan sulfate connected to the protein sydecan to form a proteoglycan complex. Heparan is a sulfated sugar (linear polysaccharide).
In part B of the figure at the bottom of the picture, you can see the coding marks on the heparan sulfate. That shows a simplified information bearing sugar molecule. In Part A, you can see how it is connected to a membrane protein called sydecan. This enables signaling and information processing at the membrane.
The exact sulfate pattern on the haparan molecule changes. That means there are numerous such information bearing patterns, and they have no mapping to the DNA.
The complexity of what happens in membrane and cell trafficking is staggering. We are only scratching the surface, and the pharmaceutical companies are forecasted to be spending tens of billions of dollars researching sugar interactions.
But, why do we have to settle the issues about this today? Larry and others in his camp want the issue to be settled today – 82.5 Megabytes of DNA is all the complexity that exists in humans.
The alternative is we could wait and see and learn more. Insistence on the 82.5 Megabyte DNA viewpoint is a science stopper, imho.
There are many more glycan patterns than depicted for the heparan sulfate. If indeed the sugars and proteins are information bearing, it would dwarf the genome in terms of how much information is there. Word got to me that Don Johnson shares Wells and Meyer’s view, but don’t quote me on that. That was passing remark, but if you ever interact with Don, you might run these questions by him.
Hi Allan Miller,
Thank you for your comments. I found this point very helpful:
You (and Sal) might be interested in this short article:
Third Genetic Code Anyone? by Geoffrey North in Current Biology, Volume 21, Issue 6, 22 March 2011, Page R203. Here’s an excerpt (emphases mine):
BTW, it seems reasonable that mutations that affect early embryonic development should be more susceptible to cause problems. Perhaps that’s the reason why we look a lot like our distant ancestors during early embryonic development stages
Nelson’s peers in the secular community look favorably on his work with Orphan genes as evidence by getting published by Cambridge University Press.
Since Dr. Joshua Swamidass broke the news already, I guess I can break the silence:
https://discourse.biologos.org/t/orfans-de-novo-genes-and-taxonomically-restricted-genes/5791
You’ll see a chapter by Nelson on Orphans. Now how in the world did a creationist get into a book like that. 🙂
See:
the chapter in question is available online as Dr. Swamidass pointed out:
https://www.researchgate.net/publication/304039133_Next-generation_apomorphy_the_ubiquity_of_taxonomically_restricted_genes
stcordova,
Thanks, but I’m not a biologist, not even a particularly knowledgeable layman and I’d rather get my biology from biologists, not a creationist philosopher like Nelson
My point was, if we find differences in HOX genes, or any genes known to be involved in early embryonic development, between closely related species, then we know Nelson is wrong in saying those mutations must be lethal
Nobody gives a shit about peoples religion if what they are producing is scientific.
Indeed. Genetic control sounds like one of those nonsense terms someone might just make up.
dazz,
There is a fair bit of copy number variation. eg https://www.ncbi.nlm.nih.gov/pmc/articles/PMC299744/, and https://www.ncbi.nlm.nih.gov/pubmed/15288047, linked earlier. This isn’t the whole genome duplication of Shapiro. One would expect to find some phylogenetic evidence of that.
That’s right. Lack of imigination v. imagined therefore real.
So much for “genetic control theory.”
Thanks Allan, much appreciated.
From that paper: “) The association of hagfish homeobox sequences with gnathostome sequences suggests that at least one Hox cluster duplication event happened in the stem of vertebrates, i.e., prior to the most recent common ancestor of jawed and jawless vertebrates. (2) The high number of paralog group 9 sequences in hagfish and the phylogenetic position of hagfish suggests that the hagfish lineage underwent additional independent Hox cluster/-gene duplication events.”
Isn’t this exactly the kind of thing Nelson claims must be an evolutionary dead end? How come did those hagfish survive those duplications?
Frankie,
Unlike you, I construct my posts to order. I don’t consider posting duelling opinions to be a particularly constructive use of anyone’s time. “Expert A says ….. [10 paragraphs out of context]” “Yes, but Expert B says … [10 more paragraphs]”.
Like I say, argument by glove puppet.
Mung,
Who has proposed that? Me? I think you may be misunderstanding me.
Like I say, computing metaphors are misleading. So if you read me as using one, allow me to disabuse you of that notion.
You construct your posts based on your unsupportable claims. You refuse to listen to any experts who disagree with you and you never show that they are wrong.
Yours is nothing more than an argument from bald assertion
Human HOXA1:
MDNARMNSFLEYPILSSGDSGTCSARAYPSDHRITTFQSCAVSANSCGGDDRFLVGRGVQ
IGSPHHHHHHHHHHPQPATYQTSGNLGVSYSHSSCGPSYGSQNFSAPYSPYALNQEADVS
GGYPQCAPAVYSGNLSSPMVQHHHHHQGYAGGAVGSPQYIHHSYGQEHQSLALATYNNSL
SPLHASHQEACRSPASETSSPAQTFDWMKVKRNPPKTGKVGEYGYLGQPNAVRTNFTTKQ
LTELEKEFHFNKYLTRARRVEIAASLQLNETQVKIWFQNRRMKQKKREKEGLLPISPATP
PGNDEKAEESSEKSSSSPCVPSPGSSTSDTLTTSH
Chimp HOXA1:
MDNARMNSFLEYPILSSGDSGTCPARAYPSDHGITTFQSCAVSANSCGGDDRFLMGRGVQ
IGSPHHHHHHHHHHPQPATYQTSGNLGVSYSHSSCGPSYGSQNFSAPYSPYALNQEADVS
GGYPQCAPAVYSGNLSSSMVQHHHHHQGYAGGAVGSPQYIHHSYGQEHQSLALATYNNSL
SPLHASHQEACRSPASETSSPAQTFDWMKVKRNPPKTGKVGEYGYLGQPNAVRTNFTTKQ
LTELEKEFHFNKYLTRARRVEIAASLQLNETQVKIWFQNRRMKQKKREKEGLLPISPATP
PGNDEKAEESSEKSSSSPCVPSPGSSTSDTLTTSH
ETA: Of course I have no idea how early in embryonic development this mutation takes effect
Paul never said that. They could be lethal, but not necessarily so.
I guess another way to approach this is through embryology. If there’s evidence of differences in early embryonic development between closely related species we should conclude that Nelson must be wrong. Do we have that?
The hype of the headlines doesn’t really align with reality. First, they published only the defects of the embryo, not a Zebrafish with actual limbs. Below is the picture of the poor creature with defective fins. Curiously, why don’t they have an adult zebrafish to showcase. Did their mutation make the zebrafish Dead on Arrival (DOA)?
As Stephen J. Gould said, “what good is half a wing”. Or to paraphrase Walt Brown, “a fin will become a bad fin before it becomes a good leg.”
There is much more to the anatomy and physiology of leg than just deforming a fin.
Contrast the picture of the deformed fin (below) with the anatomy of a functioning leg:
http://images.medicinenet.com/images/illustrations/anatomy_legs.jpg
The reviewers who passed this article show eagerness to dump critical thinking in favor of narrative that really doesn’t agree with facts.
Lethal or deleterious, an evolutionary dead end anyway
Based on a reading of the chapter, by carefully suppressing any notion of creationist claims or hypotheses and by appearing to accept common descent as a reliable inference from data. Do you think that chapter has some kind of hidden message? If so, what could it be?
Thanks for posting the sequences. It shows how similar we are, but if I may point out, that looks more like the protein sequences, not the DNA sequences.
The protein sequences definitely mask differences in the non-coding regions. So the comparison is a bit biased that way.
Also, I don’t really trust the Chimp gene assembly. The supposed “de novo” assembly wasn’t really de novo. It took chimp sequences and slapped it on a human scaffold, not a de novo scaffold. So we really don’t know.
stcordova,
Yes, those are obviously protein sequences.
The point wasn’t to show the similarity, but to put to the test Nelson’s hypothesis, but since I have no idea if that substitution effects early embryonic development I don’t know if it’s relevant or not
stcordova,
I googled ‘chimp human scaffold’ and the 1st answer was … In Genesis! Referencing (in 2013) something written by one Richard Buggs in 2008 based upon draft sequences. It is now 2017. Did the Chimp project just stop?
Certainly not. Here are the details regarding the assembly of the current (3.0) chimp genome release (from https://www.ncbi.nlm.nih.gov/assembly/GCF_000001515.7/#/st):
While the chromosomal version of the assembly makes use of the human genome to aid in identifying chromosome breakpoints, the scaffolds themselves are de novo assembled.
From one of the papers that Allan linked earlier:
A mechanism for punctuated equilibrium?
I don’t read it that way, but this will induce me to make some phone calls. Thank you very much for the different take. Thanks again!
Perhaps a better avenue, just a guess, is what is written by medical researchers. The following had something interesting at the end regarding genetically engineered mutations in mice Hox vs. human Hox.
http://www.sciencedirect.com/science/article/pii/S1096719213003600
From the paper cited, mutating Hox1A can be bad juju:
The list goes on, but that’s a sampling.
stcordova,
You’re welcome, Sal, but I’m curious in what way you do read it, then. To reiterate, here are the methods used to assemble the 3.0 scaffolds:
At one point in that process do you see human genome being relied upon?
stcordova,
Yeah, yeah, I know most mutations there are highly problematic for obvious reasons. How many possible deleterious mutations in HOX genes can you cover before we conclude that EVERY possible mutation there is lethal or deleterious?
I think the answer to this “issue” is incredibly straightforward. Can we tell the difference between a human embryo an a chimp embryo in the early stages of development? If the answer is yes, then it follows that modifications in early stages of development have happened since the divergence. We also know the sequence similarity between humans and chimps means this only took a few mutations in HOX genes, and only a subset of those would effect early development stages. Pretty sure this is a clear falsification of Nelson’s hypothesis that these changes are out of reach of known evolutionary processes
dazz,
I’m for substituting the opposite gene in each species and seeing what crawls out … if I can get permission from the ethics committee! Don’t blame me if it all goes horribly wrong and we end up being their slaves.
Hmmm…I feel like I’ve seen a movie about this…
LOL, pretty sure you would get…. a crocoduck!, because, you know, there’s much more to it than DNA.
BTW, can I ask you if my objections to Nelson’s argument make sense please? Am I missing something here?