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.)
Looks like a dancing cow. Now I want to use that picture for my avatar.
Actual proof that the DNA arose by Random Mutation and Natural Selection. Wow!
hahahaha, good catch.
dazz,
I’m no expert tbh, but it seems to me that Nelson is effectively trying to prove a negative. Most mutations can be detrimental, but evolution could still proceed by the ones that aren’t. In the case of HOX, they are highly conserved … evolutionarily conserved, if one believes that kind of nonsense(!).
If they are evolutionarily conserved, it means that non-detrimental changes to them are quite rare. This does not mean non-existent. And certainly, the human and chimp ones seem a very short step apart. Neither species has arms growing out of its head, or whatever. It may well be that the difference has no impact on development in any case.
Allan Miller,
Thanks Allan
Here‘s another cool paper (there are loads!). Particularly figure 2. The most important bit of a human – to the human – sits beyond the region that controls the development of the mouthparts in Drosophila. There is something both unsettling and cool about that.
[eta: “Evolutionary conservation provides unlimited scope for experimental investigation of the functional control of the Hox gene network which is providing important insights into human disease. ” The hell they say!]
Evolutionarily conserved is an oxymoron.
shhh, that’s one of the secrets that the evolutionist materialist establishment doesn’t want us to know
Allan Miller,
Holy shit!
Here:
That’s sort of bad imho, if one is making the case for Chromosome 2 fusion of humans from the Chimp ancestor.
Wow! All you need to turn a fly into a human is to stick on a different head and neck.
Praise the Lord!
Now seriously Mung, have you been following the thread? Do you agree with Vincent about the inevitable saltation that must have happened if the proposed arguments are true? just curious
Excellent depiction of common design optimized for scientific discovery. We have a creature with an exoskeleton and on with a endoskeleton controled by the Hox genes.
https://en.wikipedia.org/wiki/Exoskeleton
https://en.wikipedia.org/wiki/Endoskeleton
The insects (like fruit fly) are protostomes. The humans are dueterostomes.
Paleontologist Marcus Ross points out the problems of characterizing the protostome-deuterostome ancestor on anatomical and physiological grounds.
http://digitalcommons.liberty.edu/cgi/viewcontent.cgi?article=1079&context=bio_chem_fac_pubs
Reminds too of PZ Meyers arguing for the common ancestor of animals and plants due to histone modifications or whatever, even though an animal-plant is a bit absurd anatomically and physiologically.
I apologize if this has already been discussed, but I am far too lazy to read through all 200+ comments.
But Axe and Meyer lost all credibility when they included number v in their list:
Only a moron would think that that is an actual argument.
I don’t get it. I noted in my original comment that the chromosome version of the assembly was aided by the use of the human genome but stated that the scaffold assembly was de novo. You disagreed with this but didn’t specify why. Now you’re saying that you disagree because the human sequences were used to help guide the chromosome assembly, which is what I stated in the first place. So where do you actually disagree?
In any case, the de novo scaffold assembly is more than sufficient to address the question that you and dazz were originally asking. For the record, it also makes perfect sense to use the human chromosome structure to aid in building the chimp chromosome assembly since the human structure is worked out better than any other mammal structure and the two species are so closely related (whether you accept this or not).
Seems like a non sequitur to me. What does the Chromsome 2 fusion have to do with whether or not the particular chimp sequence that dazz posted is reliable?
https://www.wired.com/2010/01/green-sea-slug/
I was kind of surprised that such a sophisticated organism could have so many characteristics of both plant and animal. I had been expecting single celled organisms, and I’m sure there are some.
And while I concede that the green sea slug is absurd, it’s also real.
stcordova,
Source? Liberty University: “Grow in your faith as you participate in the wide variety of ministry and mission opportunities at Liberty University.”
“Get a world-class education with the solid Christian foundation you’re looking for at Liberty University. Here, you’ll gain the values, knowledge, and skills you’ll need for success in every aspect of life.”
Sorry Sal, but this deserves a big fat
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DERP.
Allan Miller,
What is the mechanism which makes some genes highly conserved?
That’s circular reasoning. It might be correct in the end, but it’s still circular reasoning. “Evidence” of chromsome 2 fusion is a Chimp assembly that is force fit using human chromosomes as scaffolds. Don’t you find that a bit unrigorous?
Regarding your other questions, maybe it doesn’t have a bearing on what Dazz was talking about, I just had to issue a general caution, so maybe you are right, maybe likely right.
Maybe you’re right about the smaller contig scaffold, maybe likely right that’s why I want to have some conversations with my colleagues, so maybe we don’t disagree, but never hurts to ask around, and maybe my colleagues can benefit from reviewing your objection.
Do you have background in assembling mammalian genomes of that size, I don’t, so I’m glad you weighed in.
I find your objection nonsensical. Evidence of chromosome 2 fusion is that the assembly of two chimp chromosomes aligns to one human chromosome. Are you denying that the chimps have two chromosomes where the human has one? Are you denying the sequence similarity that allows for alignment? I don’t understand your objection. How could this be illusory? What other explanation than chromosome fusion can you advance?
The reality:
Contrast with the popular press:
I should point out, chloroplasts are those things with structural inheritance. Something I talked about earlier. Maybe sea slugs demonstrate we can transplant plant organelle’s into animals. Bwahaha! Which would of course confirm non-DNA structural inheritance.
I do not understand this problem. Can you explain it? We would expect some characters of the ancestor to be those of modern protostomes, some to be those of modern deuterostomes, some to be intermediate, and still others to be none of the above. Where’s the problem?
I doubt that PZ did any such thing. Of course you must realize that the common ancestor of animals and plants was a single-celled protist without chloroplasts, right? Again, you will have to explain how this is in any way a problem.
But since you ignore almost everything I ask you, you probably won’t.
No, I really don’t. AFAIK, there are many lines of evidence pointing to the fact that human chromosome 2 is a result of an ancestral fusion. This was known long before the chimp genome was sequenced (see this paper from 1991 for example: http://www.pnas.org/content/88/20/9051.full.pdf).
I’ve more relevant experience with de novo transcriptome assembly, but not I’m totally unfamilar with assembling genomes.
Yeah, guilt by association is hard to overcome. You might consider at least hearing the arguments in that paper.
On a smaller note, how reasonable is it a creature with an endo skeleton emerges from one with an exoskeleton and vice versa. The organs (like digestive one) in mammals are outside the endoskeleton, whereas in insects it is inside the exoskeleton. That transition seems a little difficult. I mean, it would be kind of hard to have a gradual transition from one to the other, don’t you think?
But we have evolutionary biologists here who should be able to describe how it can be done from a mechanical standpoint. Like rewiring how the nerves and muscles and respiratory and circulatory organs and one day be inside the creature and then hanging out the next.
This is one example why I think common design optimized to help humans understand themselves is a better explanation than common descent with mindless modification.
Do creationists never get tired of the crocoduck argument? The common ancestor of insects and vertebrates had no hard skeleton at all. At most it had a hydrostatic skeleton. There was no gradual transition from one to the other; there were a gradual transitions from no skeleton to a skeletion, twice, in separate lineages. We have fossils of some of those transitions, and there are living organisms that display some of the transitional stages. Stop reaching for zingers on subjects you know nothing about, unless you like embarrassing yourself.
Why?
VJT made a similar claim regarding the distribution of complex adaptations and all people could do was ignore it or mock it.
Pot. Kettle. Black.
I just can’t wrap my head around this. I mean, Sal obviously has studied biology a LOT more than I have (which is not saying much, but still, he obviously has put a fair amount of time in it and it shows) but even I see why those must have been separate evolutionary pathways, one leading to an exoskeleton, the other to an endoskeleton. It just makes sense.
Religion poisons your intellect kids, and YEC obliterates it
Because that’s what we would expect from diverging lineages maybe? It’s not rocket science FFS
What I have observed is that you appear to rather regularly misread VJT’s comments and thus misrepresent his views. In the most recent case I didn’t say anything because at times I get tired of correcting you. So I’m not going to say anything about what VJT thinks.
I will give you my own opinion though, when it comes to matters of saltations. They are a fact. So the sooner you get over your antipathy towards them the better.
I don’t know what it takes to create an animal. I typically don’t much care to get involved in those sorts of arguments because I don’t think the fans of evolution can even explain what it takes to make a simple cell.
No one knows. We may never know. And none of us has the science on our side. We believe what we believe for reasons unrelated to what science can tell us.
Perhaps some humility is in order. That’s my thinking.
So your opinion is a fact. Interesting. Care to share what makes you think saltation is a fact, what saltation(s) in particular and what’s the evidence that makes you believe that?
Pot. Kettle. Black
I will give you two. Whole genome duplication, mentioned earlier in the thread, and symbiogenesis. I can probably come up more, but let’s see how you handle those two.
Now, please tell us what you think deserves to be called a saltation and what does not. Because, you know, you’re so freaking certain that they cannot happen.
Interesting post over at ENV.
Digging Deep in Biology
Oh, and to make sure I don’t do what you constantly do, let me admit I’m guilty as charged. But also let me point out that I told you that those “misrepresentations” weren’t intentional, and that I also told you that they didn’t make a difference and my objections worked all the same regardless. Vincent has acknowledged (I think) that there’s no way to reconcile these “edge of evolution” type of arguments with common descent unless wild saltation (sic) events are assumed. He said he believed that the vertebrate transition must have been one of these “wild saltation” events.
I don’t think you’re following. Again, WGD observed in yeast didn’t imply any kind of saltation. What I mean by saltation is a “massive” phenotypical discontinuity in a single generation. “Hippos giving birth to whales” so to speak.
So, phenotypic change without any corresponding genotypic change.
No one, except you, knows what qualifies as a “massive” phenotypical discontinuity. And I’d wager that no one, except you, think these happen without changes in the genetics.
Certainly not VJT. Try again.
Is that because yeast don’t have a phenotype, therefore there was no “massive phenotypical discontinuity”?
The massive phenotypical discontinuity follows from the argument presented by Nelson (and any other similar arguments like IC, Functional Coherence, etc..), which implies that there’s no gradual, genetic pathway available to evolution to produce the transition. Do I have to spell it out for you AGAIN?
WTF? Have you considered that maybe WGD doesn’t have a (significant?) phenotypical effect, and therefore can’t account for any kind of saltation?
That would imply that the saltations are genetic.
Yet you’ve also said:
I’m just asking what you think qualifies as a saltation. Hippo giving birth to whale? Is that your final answer?
Why can’t saltations take place at the genetic level?
And when will you address symbiogenesis? Do you think there was no phenotypic change involved? Therefore not a saltational event?
fwiw, the index of Sean Carroll’s Endless Forms Most Beautiful has no entry for body plan or bauplan. I’m sure there’s a perfectly logical reason.
Mung,
I’m gonna pass Mung. I’ve had enough of this. If you want to go back and check one of the DOZENS posts where I made my case let me know what you think.
This is exactly what evolutionary theory predicted, so why was it “astounding”?
How do these similarities explain the differences, according to THE theory of evolution?
Sure. Please point me to the first one in which you define what you mean by a saltation. Was it the one where a Hippo gives birth to a Whale?
Why? No one expected to see such sequence similarity. Why did no one expect to see such sequence similarity? Did it have anything at all to do with evolutionary theory?
If this is something that was predicted by the theory, or entailed by the theory, then why was such sequence similarity just stunning?
Apparently this is something neither predicted by nor entailed by evolutionary theory.
Or no biologist understood evolutionary theory.
Not predicted by evolutionary theory. Not entailed by evolutionary theory.
The 10% functionality figure, that Larry “82.5 Megabytes” Moran throws around, could be wrong as demonstrated by recent lab work on Alu elements.
Alu’s are dispersed repetitive elements. The evolutionary reasoning goes something like this:
That line of reasoning seemed unassailable probably for several decades, but the power of primate Alu elements, particularly in humans lies in it’s role in creating RNA transcripts for the transcriptome. Through ADAR mediated Adenosine-to-Inosine editing, Alu RNAs (generated from Alu DNAs) can be edited, and in fact an estimated 100 million Alu RNA sites are editable. Furthermore they are in pairs that create dsRNAs and circular RNAs. We don’t know exactly how they work except when ADAR editing in mice is shut down it either results in brain seizures or death! Since it would appear the Alu structure is needed for enzymes and other molecular machines to bind to it in order for it to be edited and used as endpoints for dsRNAs, one can see the entire Alu is functional, thus 10-11% of the human genome that is made of Alus is likely functional. Furthermore, Alu RNAs in humans undergo twice as much A-to-I editing than in chimps.
It would appear the Alu RNAs implement some sort of EPROM or RAM in connection with dsRNAs to create regulatory or some other kind of mechanism.
So, again, I plead with VJ Torley, not to let what Larry says be the final word on so many things. The game is way too early for Larry to make sweeping pronouncements, especially in light of the fact his views are increasingly marginal in the mainstream.
Below is my discussion on Alus, and the comments got better toward the end since I piled on more and more citations. Even in the face of all this empirical evidence, is Larry been willing to reconsider his number could be wrong and that future experiments on Alus could overturn his beliefs?
By golly that was the best criticism I’ve gotten all day. Thank you.
So I must fall back on Marcus Ross and Paul Nelson’s problem of the Uber Bilaterian instead.
So that you can avoid the implications of the evidence by moving the goalposts yet again?
Yes, that’s the ID way.
Glen Davidson