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.)
Mung and Alan Miller,
You may be interested to know that Behe writes on p. 197 of his book, The Edge of Evolution (The Free Press, 2007): “Types of animals that have the same body plan are generally grouped together in the same phylum…”
Sal,
How much source code do you think it would take to code for a human being? I’m just curious. By the way, thanks for the pictures and links relating to embryogenesis.
Colewd,
With regard to the figure of 100 billion trials which you cite: there would have been more than enough time for those. Dryden, Thomson & White estimate that up to 4×10^43 different amino acid sequences could have been explored since the origin of life, which would imply that if life originated within the first 100 million years in the Earth’s four-billion-year history, as is now believed, then about 10^42 sequences would have been explored. In Dr. Axe’s book, Michael Denton is quoted as estimating the number of possible protein sequences that could have existed on Earth as 10^40 (pp. 30-31).
dazz,
I didn’t say that I buy Paul Nelson’s argument. Currently I’m agnostic in my views on that particular argument.
Let’s demystify it a little. Blue eyes are never inherited. Neither sperm nor egg nor zygote has blue eyes, or any eyes for that matter. But of course you know how inheritance works for blue eyes. What if histone modification works the same way? What if differences in DNA sequences determine the differences between species (and many of the differences within populations)? That would certainly solve the inheritance mystery, wouldn’t it?
UD says epigenetics is trivial?
I don’t think so.
Can’t be done. That would give you a mindless zombie, not a real human.
And yet humans and other primates have different body plans. Horses and whales have different body plans. Fish and mammals have different body plans.
It is not source code, but bits of information (information in the qualitative information). I would guess in the vicinity of peta bytes (10^15 bytes) based on the published numbers on brain complexity alone. But that is a side discussion, I’m focusing on what we’re actually discovering in the lab in terms of the information we see in the cell (like the rapidly changing epigenetic methylation patterns in embryogenesis).
We don’t know exactly where the develomental/assembly instructions are, a growing minority think the developmenta/assembly instructions are dispersed in the cytoplasm, not the DNA. Some think the assembly instructions are orders of magnitude larger than then DNA, hence the extra information must not be stored in the DNA.
Meyer and Wells argue vigorously that the surgar code system (in the form of glycans) takes precedence over DNA in terms of inheritance. People tend to think DNA is the primary source of heritable information because we can mutate it and get a radical change, but we can’t seem to do the same to the cytoplasm. But that could also mean the cytoplasm’s information is so deeply redundant it doesn’t have single points of failure like DNA, it doesn’t mean the cytoplasm isn’t information bearing. The organelle inheritance as illustrated the mitochondria illustrates the idea of deep information redundance that doesn’t have single point failure like DNA.
The sugar coding system dwarfs DNA in its information carrying capacity. But proteins themselves are information bearing!
One such class of proteins are the histones themselves. Depicted below are histones (H2A, H2B, H3, H4, H1) with tails. Note the little flags or decroations on the tails. Each decoration represents one amino acid that can be modified (like a bit being switched on). These bits can be read and written to. Histones are only one class of proteins, but other proteins can have comparable modifications. That means proteins, particularly in humans, are information bearing! This also shows the importance of individual amino acids on the protein. The amino acids are frequently dual use: one to do the work of proteins, the other is to maintain bits of information. Histones for example help structurally, but the individual amino acids are used for information storage. Those modifications are a subset of what is known as post-translational modifications of proteins.
And as I tried to show with respect to organelles like mitochondria, critical information to construct the organelle is not solely in the DNA, but the organelle itself provides the copy-and-paste template! That means the copy most likely of the posttranslational modifications to proteins, their location in the mitochondria, the glycans conjugated to the proteins, and who knows what else.
Larry said information on histones is not inherited. It is way more subtle than Larry is letting onto since we see histone information appear generation after generation, and when that information is compromised, it often results in sickness or death. It is not inherited in the simple copy-and-paste manner of DNA, but it is inherited by far more complex unknown means, otherwise we would be dead.
You are welcome. Please ask more questions on these topics. Much as I respect the fine mind and learning of Larry Moran, statements like “methylation is trivial” distort the actually complexity involved.
The methylation patterns are different for each cell, and it is believed that is critical for cells being able to identify themselves during development (bone cells from skin cells, skin cells from nerve cells, etc.). That is non-trivial. No one knows how those patterns are inherited from generation to generation since it bypasses copy-and-paste duplication on the DNA itself during germline transmission. Ergo, I think it is non-DNA inherited through the cytoplasm by yet-to-be discovered mechanisms.
Please ask, and I’m happy to walk you through. These are conversations worth having. It’s easier to learn than you think, you just need to learn some buzzwords and unlearn the way Larry is trying to teach epigenetics!
FWIW, I was not taught epigenetics the way Larry is teaching it. I learned what I’m sharing with you through numerous visits to the NIH in the form of classes and seminars open to the public. I live within commuting distance from the NIH where the ENCODE and RoadmapEpigenomics consortiums have their central management offices, so I’ve been familiarizing myself with epigenetics ever since I attended the 2015 ENCODE conference.
Visiting the NIH opened my eyes to how truly marginal Larry’s views are relative to the views of the medical research community represented by the NIH ENCODE and RoadmapEpigenomic consortiums. One will get a distorted view of these issues by visiting Larry’s blog and even UncommonDescent.
I’m trying to remedy these distortions by reporting on the way the NIH’s half-billion dollar research into the epigenome actually conceptualizes the epigenome.
You’re agnostic about it? seriously? So even if it follows that if Paul Nelson is right, then body plans must have suddenly appeared fully formed which means for example that bilateralians were born off some drastically different creatures with different body plans?
Don’t you think this is an issue worth considering? I would say this alone is a VERY good reason to be highly skeptical of Nelson’s claims. And also Axe’s claims about functional coherence for that matter, and Behe’s IC, since the same reasoning applies to those too.
I seriously hate to repeat myself like this, but if one questions that evolution can produce the observed life diversity through known gradual mechanisms of mutation, selection and drift, then the only alternatives are special creation or wild saltation (if one accepts common descent). If we’re gonna have an honest debate about this we can’t just sweep this under the rug.
All this ridiculous “edge of evolution” type of arguments need to stop, or else admit you’re just spinning the same unscientific apologetics as the rest of IDists
This can also be powerful evidence of pre-meditated design to help with the process of scientific discovery. Better that we can learn about developmental pathways by experimenting on zebra fish than human embryos.
It’s so much easier to learn key aspects of the epigenome by studying yeast than working only with humans. It’s so much easier to learn important things about DNA transcription and translation by studying bacteria than working only with something more complex like the eukaryotic architecture of humans.
The patterns of diversity and similarity are almost spooky in how well they are optimized to help us understand biology. It’s like God left a trail of machines to help us understand ourselves.
Why?
It’s easier to see their insides.
vjtorley,
This is exactly right and if all proteins had to do is bind ATP, and proteins were limited to 80 AA, then evolution by trial and error might be possible.
In the Axe experiment when the requirement was to bind to another protein and the break down a molecule the number went to 1/10^77 for a 150AA protein clearly outside Denton’s limit.
Most proteins in modern eukaryotic cells must bind to multiple proteins. Binding requires AA sequence precision. This is validated by the action of the human adaptive immune system.
VJ,
An additional consideration as to why I think “God optimized design to help scientific discovery” vs. common descent are diagrams of genes like the following.
Most certainly humans are similar to chimps than to trees, but we have lot’s of things that make little sense in terms of common descent but do make sense in the “God optimized design to help scientific discovery” viewpoint which I hold. The following diagram from
http://www.sci-news.com/genetics/article01036.html
reinforces those sentiments. I had lunch with Paul not too long about to talk about his Orphan gene work. I pointed out, diagrams like the following would be in the interest of creationists to pursue even beyond the orphan gene project.
If creationists can make more diagrams like this, it will strengthen the case for common design over common descent. Note the common design in Humans and Zebrafish that are not shared by humans and mice, etc.
When I was at ENCODE 2015, I was amazed at presentation on attempts to cure kidney illness through technology developed studying Zebrafish. Incidentallly, the work leveraged a lot of the data from the RoadmapEpigenomics and ENCODE.
This is a video of the 30 minute presentation. It might give a little different perspective on ENCODE and RoadmapEpigenomics than the picture Larry Moran and Dan Gruar are painting. It also highlights how important zebrafish are to treating the human condition. I think the similarity is a gift of God, not the product of common descent.
Also, Vincent
No, Vincent. If that was the case, then there would be no evolutionary pathway between body plans. Common descent would be false if necessary mutations were invariably deleterious: organisms would be stuck in their original body plan, this is going full retard YEC.
And if these mutations can only reduce functionality, it gets even worse. Do you think that LUCA had all the functionality we see in ALL extant living forms and whatever is to come? Actually, why are you or Nelson talking about “functionality” instead of body plans all of a sudden? Because it’s obviously impossible that the common ancestor of two species with vastly different body plans had both body plans, and LUCA had ALL of them. This is so obvious that it boggles the mind that you or anyone else could credit this BS as “one of the best critiques of neo-Darwinian evolution that I’ve ever seen. Devastating is the only word I can use to characterize it.”
stcordova,
How is “common design” even an entailed prediction of anything?
It’s senseless as an explanation, since the whole point of cladistics is that “common design” doesn’t happen to exist beyond what common descent actually does explain. But it’s impossible to see how “common design” is an expectation of theistic design beliefs (which ID/creationism sensibly are comprised of) at all. It’s a limitation on omnipotence/omniscience, so at least not expected–at most a possibility.
So it fails all around. Common design is not a prediction of any design that could be the result of omniscience, and the whole point of cladistics is that commonality happens to fit the pattern of common descent, while innovations in separate lines are not common to those separate lines, except as a matter of inherited possibilities.
Glen Davidson
dazz,
Your point is well taken but not everyone in the discussion has a hard ideology they are trying to confirm like fundamental christians or strong atheists. VJT is a theist but is also comfortable that evolution maybe part of the overall plan.
Your point excludes scientists like James Shapiro who think there is engineering in the cell that can support evolution.
dazz,
What is being ruled out here is common descent by a semi random or trial and error mechanism. If a non random mechanism can be discovered common descent is still in play. This one of the hypothesis of the third way guy like Shapiro.
stcordova,
I wish you would explain what you think that diagram showing the various gene overlaps means, rather than just presenting it as proof of whatever you’re saying at the moment. Apparently it’s proof both of separate creation and common design. Zebra fish were created so as to give us a good model of human development? Hey, wouldn’t the easiest way to do that be to make them descended from a common ancestor and just retain most of the same genes and developmental pathways?
You get all that, apparently, because there are 73 genes uniquely shared between humans and zebra fish. But there are nearly twice as many uniquely shared between chicken and zebra fish. The clear message from that diagram is that zebra fish were created to help us cure chicken diseases.
It’s an entailed prediction of Linnaeus’ archetypes.
In order for Common Descent to hold any water it has to account for the anatomical and physiological differences observed between species.
Look, evolution is supposed to a theory of CHANGE. So why do you insist that the evidence for it is with the SIMILARITIES?
Well John until you can account for all of the differences between humans and fish you don’t have a scientific concept of Common Descent
And I’m showing why the arguments used to do that fail miserably. Bill, you can’t follow the simple logic involved, just stay quiet please
In humans common descent is often semi random and/or trial and error
colewd,
Everyone take a drink. Creationist mentions Shapiro.
dazz,
Your logic is flawed because you are not exploring all the alternatives. If A then B only works if C is not involved.
stcordova,
And where did they originate? This inability to follow pathways more than one step long is characteristic.
What do you get if you transfer DNA into a cell of a different species? Some developmental chimera? Hardly.
If all mutations in the genes that control animals’ body plan are deleterious, body plans can’t evolve, with or without “guidance”. Is that so fucking hard to grasp Bill? For someone like Vincent, who accepts common descent between species with different body plans, this has obvious implications and the only reasonable way out is to admit that the premise is false. Try Bill, try to understand, try real hard!
Frankie,
Ask the God Of Hagfish. Ask him why the heck he needed to screw about with their development in a manner that is simply achieved by the observed mechanism of duplication.
How did you determine gene duplication is a blind and mindless process? Talk about begging the question…
If it is a totally different type of organism nothing will develop.
What about ancient proteins? A then B only works if C is not included
Frankie,
Would you seriously expect me to dump the entirety of the genome here at TSZ, and all metabolic and developmental pathways? Even the known stuff would take a lot of bandwidth, and would prove very little, because you would say I haven’t included the ones that aren’t under genetic control. Well, duh, there aren’t any.
No, here’s an easier way, someone who thinks that there is a non-DNA system: show how it excludes DNA. Show how it manages to work without the involvement of DNA.
Because all the evidence so far is that it all roots in DNA – even small molecules and methylations etc; they are done by gene products. Until someone finds an exception, that’s the current paradigm, tough noogies.
Frankie,
How far different is ‘totally different’? The fact remains, if ‘development’ is in the cytoplasm, none of it has any influence whatever. If anything develops, it’s the DNA donor, not the cell donor, that emerges.
Except DNA doesn’t do anything without a suite of existing proteins, ribosomes, etc.
So actually, the evidence so far is that it all roots in the cell.
Dogs and cats; dogs and horses; hippos and whales
There isn’t any evidence that DNA determines what will develop
Frankie,
Talk about misunderstanding the logical fallacy…
Gene duplication is routinely observed. If you are saying that gene duplication is under direct control – that would presumably include those that led to cancer – well, you can think that if you like. I don’t. It sounds a stupid position to take.
How do you know every atom isn’t being pushed around by pixies?
dazz,
You are assuming the change process is mutation. The change process could be the insertion of a pristine functional gene from a NGE process.
Mung,
The source says ‘usually phyla’, so I’d say it hedges somewhat.
But a phylum is not quite a hard and fast rule, and one can, if one perceives the need, apply it lower. It’s that semantic thing again. The words we choose, and the discreteness or otherwise of our categories, don’t bother biology much.
That said, I can’t make much sense of the ‘baramin’ idea that these are defined by ‘body plans’ at Family level. There is a goose/duck body plan, and a Diver body plan, and an ostrich, and a cassowary … and no way can you change ‘body plans’ like that!
newton,
If there is such a thing as ancient proteins and they bind to only one other protein then how they become modified to bind to several other proteins is quite a mystery.
That would mean that there are genes without an homologous counterpart in some other species . We KNOW that didn’t happen, Vincent knows that, just stay quiet Bill, pretty please
Frankie,
Complete bollocks.
colewd,
Evolution News and Views covered protein binding in December. And now here you are pushing it! What a coincidence.
Wow- what a totally devastating rebuttal!
Do you know of any evidence that says DNA determines what will develop? There are geneticists who say they knew decades ago that although DNA influences development it doesn’t determine what will develop. I have read Carroll’s evo-devo books and he didn’t say that DNA determines what will develop. So what do you know that developmental biologists and geneticists don’t?
You just have to know HOW. But first you have to know what makes the body plan what it is- what determines it
Besides, why should we believe that a tiny mutation must always be deleterious in DNA involved in early embryonic development because it affects the whole process, but a brand new gene insertion, that would presumably disrupt the process even more is beneficial? Oh! of course, that’s just how almighty rolls
There is an acronym for it ,ASR. I think unraveling mysteries is what science tries to do.Google Thornton
Indeed.
Strange. I don’t remember balking.
AdapaPRATT?
But, but, evolution does not need to do an exhaustive search and in fact does not do an exhaustive search. So the size of the space is irrelevant.
Or so we are told by certain commenters here at TSZ.
dazz,
Dazz, are you really claiming that there is no such thing as de novo genes?
Allan Miller,
Since we have been discussing this for 6 months do you think I have a legal claim 🙂