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.)
dazz,
The clue is in the title. Design
It can’t be a default position if it is reached after considering other alternatives. ID doesn’t require the supernatural and Intelligent Design doesn’t have any fantasies.
Did scientists just throw up their hands and give up when trying to find non-telic explanations for Stonehenge? No, they went on investigating, figured out it was manufactured by intentional agencies and studied it as such so people will have a proper understanding of it.
There comes a point when it is obvious that those proposing blind and mindless processes for the diversity of life have to ante up and figure out a methodology to test that claim. They have to stop whining about ID and make a case on their own. If ID didn’t exist they still wouldn’t have anything to say in support of that claim.
The same goes for DNA. The only reason anyone can question the claim that DNA is the do-all molecule of life is because no one has ever supported the claim that it is. DNA doesn’t do anything without pre-existing proteins, ribosomes, tRNAs, etc. It’s a package deal.
That”s exactly what a default conclusion is. Settling on something by rejecting alternatives. The problem is that there is no way to know whether a list of alternatives is exhaustive. You have to allow for not knowing. As KF is fond of remarking, “every tub must stand on its own bottom”.
ID doesn’t have a scientific theory or a hypothesis.
What have the on-going and very informative archaeological investigations at and around Stonehenge to do with ID baloney? (The question is rhetorical, BTW)
Now Trump’s in charge you can throw away that figleaf.
Nobody is making that claim. The claim in comments above is that DNA in zygotes (and in the maternal cytoplasm in the egg such as mitochondria) of sexually reproducing organisms must contain all the heritable information for growth and development.
That seems to be true today. It may not have been so with the earliest life-forms.
No, it isn’t. The default is not even considering any alternatives
Straw man- that is why science is tentative Alan. It isn’t about absolute proof
I have shown you the hypotheses, Alan.
Yours doesn’t have a scientific theory nor any testable hypotheses based on the proposed mechanisms
The baloney is all yours, Alan. The point is saying intelligent design is not a game stopper as you try to make it out to be
Allan Miller- I bet John H does too
What earliest life forms? Your imagination and your position’s need are not evidence
https://www.merriam-webster.com/dictionary/default
a : a selection made usually automatically or without active consideration due to lack of a viable alternative
Then don’t.
I know that ectoplasm is used in ameboid locomotion, but I didn’t know of its use in their copulation. Who’d have thought it.
We test this by looking for their(formative principles) effects on living form.
I know that an understanding of these things requires an expansion of thinking. It involves thinking that is not restricted to an understanding of reductive pointwise forces. If you can get your head round projective geometry and realize that there is a compliment to the Euclidian space which we are so used to dealing with. Euclidian space requires the plane at infinity in order to make sense. The compliment to this which is very rarely considered is the surrounding planewise forces which require points at infinity. A sperm contains one of these points at infinity.
Most of us will have seen videos of chrysalis formation. There are plent of them on Youtube. Notice how the shell of the chrysalis forms under the skin of the caterpillar before its insides are turned to mush. This shell is molded in the shape of the as yet unformed butterfly. The form of the butterfly takes shape from the circumference inwards.
A compass needle aligns north to south. Would you say that the forces involved are all located within the metal or does the magnetic field of the earth plays a part? It is the surrounding forces of the earth which moves the needle. In the same way it is not beyond possibility that the peripheral forces affect the zygote. The earthly forces raying out from the centre can be seen as straight lines, the planewise peripheral forces are spherical in nature. Our human form begins as a sphere and we take on more of a straight upright form as we mature. Compare the bones of the head with the limb bones and you will see which forces predominate in their construction.
We can either follow the Darwinian lead, explain away the various forms as accidents of evolution and leave it at that, or we can look and try to understand why certain forms occur. We can follow Goethe’s lead and begin to read the script of nature. We gain more knowledge by following the second path.
Something tells me you’ll have great difficulty in justifying those beliefs.
Yes we all know that DNA is inherited. But DNA is not the sum total of what is inherited. What is passed on is a single celled living being. This being uses its DNA to fashion its development using the material provided by the mother.
Jaap van der Waal, embryologist:
You ask for mechanisms. The mechanisms are the same mechanisms that we all agree on. The difference is that you believe DNA instigates its own activity like Baron Munchausen pulling himself out of the mire by his own pigtails. I believe that the organism controls its own genes. The mechanisms are used by the organism, DNA does not have the power to control any mechanism. The organism works as a whole or it doesn’t work at all.
Ok,
Here is more on organelle inheritance. The researchers involved are
James Shorter at Whitehead Institute and Graham Warren at Yale
The good stuff is behind the paywall, but that was one of the more important paragrahps. Note, de novo (from scratch) assembly is flawed. That means, assuming DNA is the sole cause of the deno assembly (I doubt it), the existing organs are structurally inherited by a 3D copy process, just as I claimed.
I will continue to look for growth of isolated organelles in vitro without DNA.
I view the following as tentative support for non-DNA inheritance of the endoplasmic rectilium :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2174540/
There you have it, DNA only coded the proteins, but the seed for the structure was pre-existing Endoplasmic Rectilium material!
To get an idea of what parts I have now established as 3D photocopied vs. inherited purely by the DNA, see the diagram below. Note, I have just linked to two papers establishing the Golgi and the Endo Plasmic Rectillium have structural inheritance outside the DNA. I’ve mentioned also the mitochondrion, but that has mtDNA, so that is a bit tougher to make the case.
I could probably find stuff for the cytoskeleton as well! Not pictured are the centrioles, but I showed that centrioles have non-DNA inheritance. But you can see then, I’ve accounted for large parts of the cell already.
Now I have stuff I can run by some researchers at the NIH when go there for biochemistry training starting in a few weeks. One of them is a specialist in the areas relevant to the papers I cited. Yay!
It seem that nobody has anything to counter what you say above, Sal. I don’t see what can be said against it. Yes DNA is passed on from mother to offspring, but so is all the other constituents of the offspring, which in the first instance is the fertilized egg.
More from the Jaap van der Wal link I provided above
And this is the case from beginning to end of the life of the individual.
Thanks Charlie M. Thanks for the links too. God bless. 🙂
The following is some really technical stuff, but I’m depositing it here in this conversation since this relates to junkDNA and development and embryology.
This comment is about insulators in DNA, and unfortunately may be confused with what Larry points out is the “Insulation theory of Junk DNA”:
http://sandwalk.blogspot.com/2015/05/the-insulation-theory-of-junk-dna.html
The “insulation theory of Junk DNA” was indeed cringe worthy, but unfortunately that sounds too similar to a real theory that deals with insolators (not insulation) theories of DNA.
Even Larry was not familiar with the term “insulator” in 2015.
I open first with this quote by Larry Moran, professor of Biochemistry:
So Larry, a textbook author, admits in August 2015 he is not familiar with this term.
I was at ENCODE 2015 a month earlier and I asked around, and some of the guys also said some terms were not well understood. Apparently this isn’t textbook stuff, but it is pretty important to understanding embryology, development and the role of junk DNA. So let’s cut Larry some slack. The insulator concept is cutting edge. But that doesn’t make it invalid, and Larry rightly points out it is going to be hard to determine function for these stretches of DNA.
But once we find evidence of function for these stretches of DNA, it inspires the belief in the possibility similar stretches of DNA are also functional! But it is brutally difficult to find the actual function, so patience is in order.
This following article relates to the what happens when DNA insulating sequences don’t work correctly (are mutated). Again, I can’t emphasize again how difficult it was to figure this out. The diagram below shows what happens with the insulator function is compromised. In this case not by DNA mutations but by “epi” mutations on the methylation patterns on the DNA. IIRC I was down at the NIH when the lady who figure a lot of this out was presenting.
The point however is showing the importance of insulators, and then this shows the importance of how genes and DNA between the genes are laid out sequentially on the genome. It can’t be willy nillly.
This is just one measly section of DNA, and the complexity just boggles the mind. The interactions are very very complex involving DNA, epigenetic methyl modifications to DNA, CTFC proteins, chromatin looping, etc.
This is a setup for some other comments. The main point is however, diseases like Beckwith-Wiedemann and Silver-Russell appear when the insulator system fails. This is helpful in understanding why it is unlikely a lot of the genome is junk, but that will be in subsequent comments.
http://dev.biologists.org/content/139/6/1045
Below is a powerful diagram of how an insulator (the reddish coils) block the enhancers (the green rectangles).
In the diagram below the linear layout of the DNA is at the top, but the 2D/3D layout is depicted at the bottom. It emphasizes again that genes can’t be willy nilly laid out on the genome, and that the sequences in between genes are functional in providing 3D positioning and acting as parking lots for molecular machines (not shown) like CTFC.
Note that genes (rectangles preceeded by flags) with promoters (the flags) can serve as either protein-coding genes or enhancers of other genes. The multi-use of genes (not just for coding) boggles the mind.
In the diagram, the genes can be green rectangles or pink rectangles, but note the green rectangle genes can serve as enhancers to the pink rectangle genes. An enhancer enahances the amount of RNA transcribed from a gene. The green genes not only eventually create RNA of their own (maybe in another cell type) but enhance the amount of RNA put out by the gene (in this case pink) it enhances. It boggles the mind how this can be coordinated so well.
It might look odd that we have an enhancer being blocked by an insulator since an insulator can block expression. But one must be aware the geometry can be every changing. The changing geometry is like opening or closing a valve of RNA expression!
Amazingly the heterochromatin also contains genes, but genes that are inactive. A lot of gene regulation is inactivation. If a cell is a liver cell, it doesn’t use the same set of genes as a brain cell, and hence has to shut those off. Genes that are turned off are often put in the heterochromatin state.
One can see form the diagram below that the DNA, in order to work, must be looped in a certain way. This looping configuration changes between cell types and thus during embryogenesis and develoment, these looping configurations have to change quite a bit. This process is non-trivial.
Sure. Notice how nobody has been on the line claiming there will not be any such functions.
To say the genome is 90% junk, and that there are good reasons for thinking it’s 90% junk, isn’t to say we know exactly which pieces are junk, nor exactly what all the 10% functional stuff is doing. We are still very far from having achieved total understanding of the parts of the genome we already think are functional.
And yes, there are going to be gray areas, where pieces of DNA predicted to be junk, will be functional, and pieces of DNA predicted to be functional, will turn out to be junk.
This idea you have gotten into your head, which you are working so hard at keeping intact, that evolutionary biologists are somehow advocating NOT doing functional genomics, is just that. Something inside your head. The closest thing you can find to someone advocating such a view are a couple of ridiculously hyperbolic statements by Dan Graur. Dan Graur’s blog and the crap he posts there isn’t “evolutionary biologists”. And a single person’s hyperbole does not the considered consensus views of an entire scientific field make.
Sure, I agree. So stop claiming this is somehow a strong indication the entirety of the genome is functional. It is not even a weak indication. Simply put, this kind of research result is to be expected. Again, some of the predicted junk will on closer inspection turn out to be functional, and some of the predicted functional stuff will turn out to be junk. And when in some distant future, we’ve found out what every functional piece actually does, we’ll have discovered the predictions were roughly correct: Approximately 10% of the genome will be functional and the rest will be junk.
The studies you link all the time, they do nothing to get you closer to your desperately sought goal of assigning function to the entire genome.
No, this doesn’t mean we shouldn’t try to find out what exactly the functional pieces are. And it doesn’t mean we shouldn’t try to find out how mutations in junk-regions can cause disease by resurrecting the biochemical activity of ancient retroviral insertions, or transposons, or creating alternative splicing sites in introns, or something like that. All of that research should still be done. What should not be done is making ridiculous and grandiose, but ultimately ignorant claims about the research when those conclusions are not supported or even implied by the data.
And religious nutters who’ve spend half their adult life blathering about how emotionally intolerable and meaningless they percieve a life without God, should simply shut up and let people without this childish need for certain conclusions, do the actual work.
None of this shit is news. I learned about this back in 2006, taking fucking high school level molecular biology. Norwegian spruce has a 20Gbase genome, it doesn’t have that many cell types. The pufferfish has no junk DNA, yet it is still a rather complex multicellular organism.
It doesn’t impact the junk-discussion. At all.
Your perpetual state of being flabbergasted isn’t a type of scientific evidence that tells us the functional percentage of the genome.
CharlieM,
I have spoken against it repeatedly. The pre-existing scaffold constrains the addition of subunits to it. The structure does not need to be generated afresh in every cell. The subunits in modern cells don’t orient unless there is a scaffold to orient upon. This is not ‘non-DNA’ inheritance. And it certainly isn’t the magic extracellular guff you were peddling the other day.
The game appears to be: repeat ad nauseam till your opponents get fed up. Then get clapped on the back for having an unanswerable position.
Funny that, on the one hand it’s not about DNA. On the other … that DNA must be doing something, surely?
Here’s a sense check for the ‘non-DNA inheritance’ crowd. If you mutate DNA, how many generations does that last? Conversely, if you perturb a structural element, how long does that perturbation last?
Ach, I’m off to reprogram a sandwich. It goes into my pre-existing structure, not my DNA. I’m not the product of my DNA, dammit, I am the product of my sandwiches. ergo DNA is not central. Chortle!
That really is ironic. Them silly Darwinists and their gene-centered views. DNA can’t do all this stuff. But all this DNA has to be functional, think of all those cell types and all those expression patterns and all those functional RNAs that this DNA has to coordinate and control so exquisitely. “It boggles the mind”.
To be fair, I absolutely agree, life is mindboggling. That’s not an argument for or against anything. I decided to switch and become a lab technician and work with cellbiology and molecular biology (and quite ironically, the lab I work in does disease related functional genomics), from having a career in IT for over 8 years, exactly because I find cell and molecular biology extremely fascinating and interesting.
But no amount of fascination and mindboggling on my, or anyone’s part, constitutes a valid argument or a piece of evidence for what the functional fraction of the genome is, or whether it was the result of an evolutionary process.
You’re so fascinated you want to tell people about it? I’m right there with you. It’s amazing. It never stops being interesting to me. But don’t use this as a substitute for reasoned arguments, or evidence. Because it isn’t.
Rumraket,
I went the opposite way, having proved myself to be all thumbs in the lab! Working in the two spheres helps me see the difference, though.
Really? Interesting
I never said I thought the entire genome is functional. A few creationists, myself included think genetic entropy has disabled a lot of function.
I do object however to a rush to judgement that something is necessarily non-functional because it rubs evolutionary theorists from Ohno to Graur wrong.
Trash talking the NIH projects like ENCODE (and by way of implication the sister RoadmapEpigenomics project) isn’t helpful, probably a little harmful.
And because I sense VJ gives a lot of weight to what Larry says (as he should because Larry is a pretty knowledgeable and smart scientist), I think he should get to hear the other side. And if we have to review every class of DNA that Larry trashes from Alus, to Lines, to pseudogenes, to lncRNAs, let’s do it.
Since VJ was bringing up embryo development, and thus by way of extension all development, let me again strongly recommend this article on insulators and developmental biology. The diagrams above were from the following paper, but it is worth reading this article as a counter balance to Larry’s ” I’m not familiar with insulator’s, but I’ll reflexively write them off as junk anyway” essay.
Well here is a chance for him and others to get familiar before he and other reflexively write them off:
http://dev.biologists.org/content/139/6/1045
The rest of the article is excellent. It provides a counter balance to Larry’s “I’m not familiar with the term, but I’ll write it off as junk” essay.
[I should emphasize again, it is unfortunate Nessa Carey mentions the “insulation” (not insulator) theory of junkDNA. For once I agree with Larry that this was an awful theory. Unfortunately it is easy to conflate with insulator theory since “insulation” is so similar to “insulator”!]
Sure it is. These organelle parts not only provide orientational templates, but Warren’s paper argues the glycan states and the postranslational modifications of proteins are also performed in the endoplasmic rectilium. So now we know maybe where the glycan templating may actually take place, at least as far as the Endo Plasmic Rectilium is concerned.
Here is a list of post-translational modifications (PTMs). Granted that DNA creates enzymes to make many of these PTMs happen, but where explicitly in the DNA does it actually say when where and how these PTMs will happen? Nowhere. That’s why frogs in a blender or cells blasted by James Tour and Jonathan Wells don’t spontaneously re-assemble. The total cellular state is highly important to conferring meaning and function to DNA, therefore it is information bearing as well and must be inherited.
I covered some of the post translational modifications to histones (like methylation) but there are so many more to histones and other proteins. No one absolutely knows where explicitly on the DNA the timing and application and execution of PTMs takes place.
At the very least, one can’t have 82.5 Megabytes of codiing and regulation, and then fail to account for DNA that creates PTMs, and that’s assuming it is on the DNA to begin with.
OK Allan and Larry, where on the DNA does it say:
Where does it say stuff like that explicitly on the DNA? That’s an important Post-Translational Modification (PTM) of a protein. Protein function isn’t just all about sequence, you know….
At the very least, if you don’t know, how can you possibly be insistent all the heritable information is on the DNA? The instruction to do what I just said are pretty important to inherit from generation to generation lest an arm grow in the back of one’s head!
And that is just one measly post-translational modification on one measly protein, and there are billions of physical (not families) of proteins that can be post-translationally modified in various contexts. Here is a list of more PTMs:
Out of interest, what difference does it make to you? Even if we discover something astounding along the lines of what you are proposing what difference does that make to Intelligent Design, YEC or you?
What must be true about biology for it to be designed? What is your point? Does YEC predict that a significant proportion of heritable information is not held in the DNA? Why? Where?
It seems the system in question would rapidly ensure such ‘optimisations’ don’t spread. So we’re left with the end result. Which is all you are considering. Which actually makes sense as you don’t believe anything was ever other then as it is now given the earth is 6000 years old, there’s simply been no time.
Wow, just wow. The argument is that DNA does not determine what will develop. DNA influences and controls development but that is not the same as determining what will develop.
How many times does this have to be explained?
He usually does, you’re the one plugging your fingers in your ears and constantly ignoring the positive arguments for junk DNA
It makes Dan Graur look like a fool. Gruar famously said, “If ENCODE is right, evolution is wrong.” My comments on Junk DNA are in support of the NIH ENCODE consortium. It means I win my argument, which counts for something personally, much like rooting for the home football team.
Self delusion is great. No one can refute Sal’s Super Bowl winning arguments
And that’s it? There’s nothing beyond that? You don’t think the designer did it one way or another?
So if ENCODE is right and evolution is wrong then what is right Sal? Or does that question not interest you?
The Endo Plasmic Rectilium is depicted below. Its structure is different in different Eukaryotes.
Of significance, as demonstrated by the in vitro experiments cited above, without DNA, but just a steady supply of necessary proteins, if the Endoplasmic Rectilium are added to the protein/cytosol soup like seeds added like seeds soil, they duplicate. Importantly in that experiment, it had a mix of protein/cytosol components from various creatures, and the EndoPlasmic Rectilium still duplicated.
As I pointed out earlier:
An Endo Plasmic recticlium from a dog pancrease was added to a soup made from:
Wheat cytosol
Membrane parts from a rat liver
Membran parts from a cow liver
Sounds almost like a magic concoction to put in a cauldron. Bwahaha!
But anyway, the dog Endoplasmic Rectilium started to grow in that environment. Not that I’d suppose it is functional, but it demonstrates the essential point that a critical organelle inherits some of its structural characteristics outside what is coded from DNA. The Dog Endoplasmic Rectillium looked like a Dog Endoplasmic Rectilium even though it was in an environment where proteins coded by the DNAs from wheat, rats and cows were involved.
It shows why it’s naive to think one can just have DNA make proteins, and like having frogs in blenders, they will spontaneously assemble to structures. What is needed for various organelles to assemble are pre-existing organelles to serve as blueprints for the next generation of organelles. This shows that for evolution to take place, the organelles must themselves have some level of evolution outside the DNA. This data demonstrates non-DNA, non-Mendelian, structural inheritance.
Brief spelling flame for Sal:
It’s “reticulum”, not “rectilium”. I say this only because you consistently use the latter term, and it disturbs me.
Getting one first down and losing by 44 points isn’t much to feel cocky about
Sure there is, but that’s icing on the cake. You have to remember, I was at George Mason University over 12 years ago where my friend, biology professor Caroline Crocker had her career ruined by Darwinists.
Darwinists tried to talk to a professor at Johns Hopkins to get me expelled from engineering graduate school where I was in an MS Applied Physics program.
It’s vindication to see these guys are all wrong.
For the sake of so many like Caroline and so many of my friends and acquaintances (like David Coppedge and the rest of the expelled), seeing the likes of Gruar make fools of themselves publicly counts for something. Same for Ken Miller, same for Francisco Ayala, same for John Avise, and especially for Daniel Denenett and Richard Dawkins.
This discussion and the collecting of the facts on junk DNA is reassurance that Graur’s fate is eventually coming. He’ll eat his words like those below. If Graur had his way, from what he is saying, he’d have these careers ruined as well, but thankfully the ENCODE crew is untouchable:
If you have a complaint about Moderation Issues you can raise it in the thread dedicated to discussing Moderation Issues with all of the other Moderation Issues that people interested in discussing Moderation Issues discuss.
I think the title of the thread is The Thread That Phoodoo Ignores, but you’ll have to Google it yourself.
OMagain,
This is Dr. Moran’s answer to Mung’s question if DNA turns out to be mostly functional.
It also may be a problem for common descent because if pseudogenes have function then the existence of the same copy of them in different species becomes less impactful evidence.
So you really think Dan Graur is right? Your comment is strong evidence of how people can be duped by loud rhetoric in the absence of facts.
Much of the establishment that actually gets lab funding and actually does experiment treat him like he’s a joke and just bypass him. But you might not get that impression since you probably just hear one side of the story.
Lab Funding for the NIH ENCODE, RoadmapEpigenomics projects: 588 milliion
and there will be more
Lab funding for experiments that Graur conducts to prove Gruar is unequivocally right: 0.00
Depicted below are a sampling of experiments that ENCODE actually conducts. Graur doesn’t have a comparable set of lab results to speak of:
Here’s what actually happened: http://www.expelledexposed.com/the-truth/crocker
I love how the Patrick just blindly accepts what others have to say about IDists. As if this person knows more about what happened than Crocker…
Sal is the miniature Tim Teebow of ID Creationism
One class of ncRNAs that Larry actually agrees is functional are microRNAs or miRNAs. miRNAs are generated from 1-2% of the genome, but it’s a little hard to incorporate it into Larry’s tally of functional DNA/RNA because many miRNA come from pseudogenes and lncRNA loci! Oh, that’s the other thing, many lncRNAs are coded from pseudogenes…..
The importance of miRNAs in establishing function for the genome however is that there mechanism is analogous to the issue with the vitamin D receptor research of Wesley Pike, it shows much of the DNA sequences are under constraint for the miRNA to bind to the generated messengerRNA (mRNA) transcripts.
That means synonymous mutations are not really synonymous at the mRNA level, the sequence of DNA really matters, and it matters in all sorts of places including (TADA!) pseudo genes.
Pseudogenes of necessity must be non-coding but similar enough to the genes they regulate. And how do they regulate the genes? By either creating miRNAs or serving as miRNA targets to regulate the level of miRNAs which regulates the level of mRNAs being translated which regulates the protein expression levels. The way miRNAs work is like a Rube Goldberg feedback control mechanism of regulation and often involves a single miRNA regulating multiple genes and creating multiple non-linear feedback control regulatory mechanisms. It puts even more functional constraint on the genome and imposes the constraints globally across chromosomes and widely separated parts of the genome.
Amazing that so many parts of the genome must be simultaneously coordinated to create a functioning miRNA regulatory network. Like Pikes work on the Vitamin D receptor binding site, miRNA binding motifs may look like randomly littered copies on the genome. Ah but there is method in this madness it leads to the ability to control many genes trough an amazing regulatory network. Here is a “simple” miRNA regualtory network that involves only 7 measly miRNAs!
That’s their spin of the facts. You weren’t actually there, I was and I know some of the guys and types of guys involved. But believe what you want, just like you believe my dad was child abuser even though you know next to nothing about him.
I’m considering becoming a pastor. The plan is teaching Jesus was a gay stripper in Sodom. Can I apply to a position in your church?
Out of interest then, what’s the first incorrect thing on that page and what actually happened? For the record.
Well, what were the facts then? Do we even agree on those?
stcordova,
Your stuff is full of statements like this! I should have started making a collection when I saw “provided powerful evidence that X could […]”.
It is not ‘non-DNA inheritance’. Sorry to disagree.
colewd,
This is pure nonsense. Common descent evidence does not depend on function.
stcordova,
That looks like a positive flurry!
How are you defining common descent?
I guess I might agree, but the question was explanation of pseudogenes. If the same pseudogenes appear in two different lineages after a supposed split then the explanation is common accidents or common design. If the pseudogenes are functional (like for reasons like miRNAs), then common design applies.
Example:
http://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-10-36
I’m sure evolutionists could find more examples if they really really tried.
The authors attribute this to convergent mistakes. Maybe they’ll see the light some day if we find that these pseudogenes are functional. I already showed one avenue by which pseudo genes are functional in eukaryotes via miRNAs. Unfortunately, I’m not aware of stuff like this for things outside of eukaryotes.
So if the same pseudogenes can converge or appear in independent lines, then there is no absolute a priori reason to invoke common descent. It is a superfluous add on of little scientific utility except as an entertaining narrative.
That’s what Patrick says!!