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.)
Is it the way that he fails even to begin to explain anything using ID/creationism that convinces you?
Or is it the way that he ignores the evidence behind evolution in order to merely criticize what he doesn’t understand?
It’s not about explaining anything scientifically for you or for Salvador, is it? While science is off teasing apart what happened, Sal bludgeons on as if science is the enemy.
Of course that impresses a creationist. Not, however, anyone wanting to learn and discover what has happened.
Glen Davidson
I too would like to thank you colewd. Those lectures are fascinating and Eric Wieschaus raises some relevant questions in the third lecture.
He has already explained that normal chemical diffusion cannot account for the distribution gradient of Diploid. Then they experimented with eggs from various fly species which were variable in size. They transplanted Diploid between the eggs and were surprized to find that the diffusion pattern was scaled to egg size.
He put three questions up on the screen:
These questions reveal the need to look beyond DNA for answers.
IMO there are two major factors in development. One is the provision of the materials required, and the other is the means by which form is established, maintained and changed during development.
DNA accounts for the first but not the second.
CharlieM,
Look, by all means. But you (the general you, proponents of non-DNA control) have to explain how these mysterious ‘non-DNA’ factors survive the haploid-diploid cycle (including 50% residence time bottlenecked by virtually cytoplasm-free sperm).
Saying ‘not DNA’ is a damned sight easier than demonstrating it.
Yet you have not demonstrated DNA is the all controlling factor.
If ID is right DNA is just the physical resource that is required to carry out the immaterial instructions that tell it what to do and when
Do we have to catch them with our tongue?
The most powerful experimental evidence to this effect is the fact when certain organelles are removed from the cell, the cell is no longer able to make copies of them. Furthermore when an cilia of a paramecium was surgically modified, the descendants of the paramecium inherited the modification. This was a very good example of a Lamarkian inheritance!
The list of organelles and parts I’ve seen so far that act as “phenocopies” for the 3D photocopying process are:
Centriole
Chloroplasts (in plants)
Mitochondrion
Endo Plasmic Rectiluim
Golgi
Cytoskeleton
Nuclear Membrane
Cell Membrane
Cilia in Parameceum
The list likely will go on.
Clearly something are not photocopied. For example the flagellum of a sperm cell in mammals. But the cilia in a paramecium is.
There is a lot to learn, but this is credible experimental evidence of non-DNA structural inheritance at the cellular level.
As I’ve also said, Larry Moran’s assumption that human complexity can be encapsulated in a mere 82.5 megabytes of DNA information strikes me as absurd. I just don’t find it believable. I suspect a lot of people, as they learn more about the complexity of a human will find that figure absurd as well.
Why? Given a omniscient designer ,efficiency in a mechanism should be unsuprising.
stcordova,
Grief, this field of ‘Lamarckian inheritance’ must have positively blossomed if people are still quoting this 1964 example of an artificially induced hair parting in a single-celled organism as the ‘type phenomenon’. I bet there are some snail coils that have gone the opposite way too. Hard to know where it will all end …
What does this demonstrate? If the canvas is removed mid-painting, the artist is left just daubing thin air. He cannot paint without a surface to paint on. Does this mean the canvas is a site of ‘control’?
Well, yeah. You put Dolly’s the sheep’s DNA from her mammary gland into a blood cell cytoplasm, nothing happens. You put that same DNA in a cell capable of germinating, it becomes a clone. What does that tell you about the importance of cytoplasmic control?
But I’m not saying your objections are without merit. What would be compelling is a interspecies transplant of organelles. I’m not aware yet of any such experiments, but I expect there is a good chance they can be done.
Felsenfeld at the NIH quotes it the textbook of my biochemistry class on epigenetics at the NIH, 2016. That’s where I found this paramecium example, so yeah, it’s still held up and example of epigenetic, non-Mendelian, non-DNA inheritance.
Though Felsenfeld absolutely detests ID, a little know fact is that before Michael Behe turned to the Dark Side (bwahaha), Behe was Felsenfeld’s post doc.
stcordova,
It tells you that you need the protein repertoire of a zygote, if you want a cell to act like a zygote. Where did that protein repertoire come from, if not DNA? It’s this flat, non-time-dimensioned thing that seems common in Creationist thinking. Point to something, don’t take any more steps back.
DNA-originated control does not mean it all has to come from that copy. DNA sends ‘messages’ to itself in time as well as space. A certain amount of the process of oogenesis involves generating (from DNA) its protein/RNA repertoire. It’s development, just as much as the somatic side.
Sure, it’s still quoted. But my reaction is is that it? It seems something of a limited phenomenon, if no more or better examples exist from more recent times.
It shows that there is ‘guidance’ from the cortical scaffold. That is not wildly different from the ‘guidance’ offered by the laws of physics to protein folding. DNA does not inform protein how to fold.
Stick a lipid molecule out of an enzyme and it will entropically fall into the nearest hydrophobic structure it can find. That’s the nearest membrane. Take the membrane away, and they fall into each other as a glob of gloop. This may raise questions re: the origin of membranes, but does not knock DNA off its perch. Lipid generating enzymes evolved in the presence of membranes.
I already posted evidence of Sal Cordova’s abuse of children in the Moderation Issues thread. I challenged you there to demonstrate that his behavior does not constitute child abuse. So far all you’ve done in response is whine.
Answer the challenge in Moderation Issues.
What convinces me the most is the fact that “junk DNA” is not junk at all and Sal puts it out as it is- the whole truth about it. You don’t like it, because it doesn’t fit into your evolutionary predictions. So, you will continue to defend your faith, bully the ones exposing it and mislead the public based on your (evolutionary) assumptions without any accountability. And that’s truth and that’s what is wrong with what you call “science”.
I had read extensively about lncRNAs and have had a pretty good idea how important they may be to the genomes. So, I’ve come to the conclusion that they had to be functional. Sal just drove the same point home beautifully with the pictures and his logical reasoning based on experimental evidence, unlike you and the rest…
For this, he deserves a standing applause!
However, the lncRNAs are just the tip of the iceberg. Here is another large field of other functional types of RNAs – lincRNAs:
Pervasive Transcription of the Human Genome Produces Thousands of Previously Unidentified Long Intergenic Noncoding RNAs
Abstract
Known protein coding gene exons compose less than 3% of the human genome. The remaining 97% is largely uncharted territory, with only a small fraction characterized. The recent observation of transcription in this intergenic territory has stimulated debate about the extent of intergenic transcription and whether these intergenic RNAs are functional. Here we directly observed with a large set of RNA-seq data covering a wide array of human tissue types that the majority of the genome is indeed transcribed, corroborating recent observations by the ENCODE project. Furthermore, using de novo transcriptome assembly of this RNA-seq data, we found that intergenic regions encode far more long intergenic noncoding RNAs (lincRNAs) than previously described, helping to resolve the discrepancy between the vast amount of observed intergenic transcription and the limited number of previously known lincRNAs. In total, we identified tens of thousands of putative lincRNAs expressed at a minimum of one copy per cell, significantly expanding upon prior lincRNA annotation sets. These lincRNAs are specifically regulated and conserved rather than being the product of transcriptional noise. In addition, lincRNAs are strongly enriched for trait-associated SNPs suggesting a new mechanism by which intergenic trait-associated regions may function. These findings will enable the discovery and interrogation of novel intergenic functional elements.
Author Summary
Much of the human genome is composed of intergenic sequence, the regions between genes. Intergenic sequence was once thought to be transcriptionally silent “junk DNA,” but it has recently become apparent that intergenic regions can be transcribed. However, the scope, nature, and identity of this intergenic transcription remain unknown. Here, by analyzing a large set of RNA-seq data, we found that >85% of the genome is transcribed, allowing us to generate a comprehensive catalog of an important class of intergenic transcripts: long intergenic noncoding RNAs (lincRNAs). We found that the genome encodes far more lincRNAs than previously known. A key question in the field is whether these intergenic transcripts are functional or transcriptional noise. We found that the lincRNAs we identified have many characteristics that are inconsistent with noise, including specific regulation of their expression, the presence of conserved sequence and evidence for regulated processing. Furthermore, these lincRNAs are strongly enriched with intergenic sequences that were previously known to be functional in human traits and diseases. This study provides an essential framework from which the functional elements in intergenic regions can be identified and characterized, facilitating future efforts toward understanding the roles of intergenic transcription in human health and disease.
<a href=
What convinces me the most is the fact that “junk DNA” is not junk at all and Sal puts it out as it is- the whole truth about it. You don’t like it, because it doesn’t fit into your evolutionary predictions. So, you will continue to defend your faith, bully the ones exposing it and mislead the public based on your (evolutionary) assumptions without any accountability. And that’s truth and that’s what is wrong with what you call “science”.
I had read extensively about lncRNAs and have had a pretty good idea how important they may be to the genomes. So, I’ve come to the conclusion that they had to be functional. Sal just drove the same point home beautifully with the pictures and his logical reasoning based on experimental evidence, unlike you and the rest…
For this, he deserves a standing applause!
However, the lncRNAs are just the tip of the iceberg. Here is another large field of other functional types of RNAs – lincRNAs:
Pervasive Transcription of the Human Genome Produces Thousands of Previously Unidentified Long Intergenic Noncoding RNAs
Abstract
Known protein coding gene exons compose less than 3% of the human genome. The remaining 97% is largely uncharted territory, with only a small fraction characterized. The recent observation of transcription in this intergenic territory has stimulated debate about the extent of intergenic transcription and whether these intergenic RNAs are functional. Here we directly observed with a large set of RNA-seq data covering a wide array of human tissue types that the majority of the genome is indeed transcribed, corroborating recent observations by the ENCODE project. Furthermore, using de novo transcriptome assembly of this RNA-seq data, we found that intergenic regions encode far more long intergenic noncoding RNAs (lincRNAs) than previously described, helping to resolve the discrepancy between the vast amount of observed intergenic transcription and the limited number of previously known lincRNAs. In total, we identified tens of thousands of putative lincRNAs expressed at a minimum of one copy per cell, significantly expanding upon prior lincRNA annotation sets. These lincRNAs are specifically regulated and conserved rather than being the product of transcriptional noise. In addition, lincRNAs are strongly enriched for trait-associated SNPs suggesting a new mechanism by which intergenic trait-associated regions may function. These findings will enable the discovery and interrogation of novel intergenic functional elements.
Author Summary
Much of the human genome is composed of intergenic sequence, the regions between genes. Intergenic sequence was once thought to be transcriptionally silent “junk DNA,” but it has recently become apparent that intergenic regions can be transcribed. However, the scope, nature, and identity of this intergenic transcription remain unknown. Here, by analyzing a large set of RNA-seq data, we found that >85% of the genome is transcribed, allowing us to generate a comprehensive catalog of an important class of intergenic transcripts: long intergenic noncoding RNAs (lincRNAs). We found that the genome encodes far more lincRNAs than previously known. A key question in the field is whether these intergenic transcripts are functional or transcriptional noise. We found that the lincRNAs we identified have many characteristics that are inconsistent with noise, including specific regulation of their expression, the presence of conserved sequence and evidence for regulated processing. Furthermore, these lincRNAs are strongly enriched with intergenic sequences that were previously known to be functional in human traits and diseases. This study provides an essential framework from which the functional elements in intergenic regions can be identified and characterized, facilitating future efforts toward understanding the roles of intergenic transcription in human health and disease.
Pervasive Transcription of the Human Genome Produces Thousands of Previously Unidentified Long Intergenic Noncoding RNAs
Enjoy!
BTW: Larry Moran; don’t forget to mention lincRNAs in your upcoming book as I’d like to comment on them in the review of your no doubt bestseller to be 😛
“” rel=”nofollow”>Pervasive Transcription of the Human Genome Produces Thousands of Previously Unidentified Long Intergenic Noncoding RNAs
Enjoy!
BTW: Larry Moran; don’t forget to mention lincRNAs in your upcoming book as I’d like to comment on them in the review of your no doubt bestseller to be 😛
J-Mac,
So you like the no-understanding aspect of Sal, of ID.
It’s common among IDists.
Glen Davidson
As a card carrying creationist, I should hope so! It shows the immutability of form, and how difficult it is to evolve things epigenetically through “epimutations” or whatever then heck we should call these things.
The real importance of such experiments for the present discussion is that it shows that 3D structures are copied directly from some of the parts of the cell themselves, while the DNA only plays a role to code the protein parts and control the cell cycle and a some other things.
I’m not contesting the value of your objections, in fact I’m saluting them.
If we see that this is also how many glycans, protein glycan conjugates, lipid glycan conjugates, maybe even RNA scaffolds in the nucleus are duplicated, then this would even further strengthen the hypothesis. Hopefully more data will come in over time.
FWIW, there are thankfully now more and more experiments related to organelle inheritance, not the least of the reasons is attempts to treat mitochondrial disease through transplantation. Though those transplant experiments don’t immediately prove the point I’m trying to make, the collective lab techniques being developed are the sort of intellectual assets that someone else might need to do the experiments I hope will be done in the future.
Until then, we are speculating in a vacuum, but I’ll stick to my guns that Larry’s 82.5 Megabyte hypothesis for the information needed to make something as complex as a human is way too small. And even supposing all the genome were functional, the resulting 825 megabytes of information therein would still seem too small to make something as complex as a human.
Indeed they don’t. Mitochondrial diseases are caused by mutations to the mitochondrial genome, and replacing that genome is what the transplants are about. It all comes back to DNA. This in no way supports your notions.
You are free to do that, of course. But be warned that intuition, especially your intuition, guided as it is by your creationist hopes, is a poor guide to reality. That’s why we have science.
stcordova,
That does not accurately represent the relationship. The 3D structures are not ‘copied’, they are extended by new molecules, which accrete upon that scaffold, not unlike extensions of a growing crystal.
You have a strange view that is informed too much by programming, engineering and the macro world, and not enough by chemistry, I fear. When one says that DNA is central, one is not saying that it specifies everything that happens down to the precise positioning of the last atom, any more than it knits proteins. The environment into which genes propel their products, and its physics and chemistry, have an effect on what happens. Indeed, what genes do depends upon those interactions existing. They don’t need specifying.
stcordova,
From the paper J-Mac cited,
This supports my observation of beta catenin and how its expression level is correlated to the cell cycle. When the cell is dividing lots of gene expression is up regulated.
The paper also supports that lincRNA expression is tissue specific and thats why their functionality has been previously hidden.
Your greater that 82.5 Mb hypothesis may have legs after all 🙂
Could anyone here explain to me WHY “noise transcripts should lack coherent epigenetic modification patterns.” This strikes me as quite the non-sequitor.
Also
This too strikes me as a non-sequitor, but of a more subtle form. Is it not a sufficient explanation that expressed genomic domains are richer in trait-associated DNA than non-expressed genomic domains? Perhaps one of the IDists here could provide a simple, in their own words, description of how GWAS are performed and what the results mean; that might help put my mind at ease here.
Alternatively, you don’t understand any of the stuff you are “citing”. [Hint: just because you ‘mention’ X does not constitute evidence that you understand X. It really isn’t “indefensible” to point out your apparent lack of understanding…]
In reality, I think that “citing” is far too kind a word to describe what Sal does. All I ever read from him are vague allusions. When asked to discuss the specifics of a particular reference, he changes the subject.
Yawn.
I don’t see anything wrong with Salvador alluding to things he may know.
You believe that this mysterious factor must have its source, if not in DNA itself, in matter of some sort. Hence it must be in the cytoplasm.
I do not believe this. I do not believe that the formative principle is some external thing hovering over the virtually cytoplasm-free sperm. They are one, they are not separate entities. The sperm is the locus, the physical manifestation of the formative principle.
And how do you demonstrate by the means of DNA the gradient in the transplanted Bicoid?. Or the inherited paramecium cilia referred to by Sal?
GlenDavidson,
I couldn’t care less… I like his killing the evolutionary nonsense… and more..
I can take care of ID inference myself.. not better than Sal, I’m afraid, but different…
Why would I want to challenge Sal? Give me one reason…I don’t need to inflate my ego though I do admit having one…
Craig Holdrige in the forward to the book, Thinking Beyond Darwin by E.M. Kranich
The genome is part of this artifact.
Where are the ID delusions berried ?
How about we start with US no-understanding what you claim?
Let’s say, each time you provide a real scientific proof for your beliefs, you get 1 point. After you move beyond 5 points without providing proof, you become the nonsense guy…
Can you handle it ? You obviously seem very confident with all your beliefs….
J-Mac,
Well, evolution still needs an explanation for where knowledge is stored from one generation to the next. How does a bird know what flying is, or a salmon know to swim upstream and spawn?
So far we have zero candidates for that role. Any DNA takers?
You seem to be searching for the biggest gaps you can find to hide your god in.
The general idea is, whatever is not FULLY understood, to your own personal satisfaction, must be attributed to your god.
(Interestingly, birds must learn to fly, just as people must learn to speak. Fish seem to work at a different level. Perhaps your god only needs to give birds a nudge, but fish a healthy push. What is your explanation?)
CharlieM,
Well, I wasn’t expecting to have to go into the area of fucking ectoplasm!
That’s wonderful. Your beliefs, however – not reallly much help. What test can these hypotheses be put to?
I believe that beetroot are the fundamental storage units of the Universe. Jupiter is made of water, but with none of its properties.
I believe that is called ‘burden shift’. It has already been amply demonstrated that DNA is the hereditary material, and from that DNA flow all the things that people have attempted to demonstrate show Other Control. I didn’t just dream this up from my armchair. If you think there are non-DNA-rooted mechanisms, you need to show what they are, and how they work. It seems to both begin and end with unicellular hair fashions from the 1960’s.
But to answer more directly: as I have said, DNA does not determine the final position of every atom. In the case of gradients, you naturally get less of something the further away from its source you are … DNA does not scuttle around putting the molecules just so.
The Paramecium example merely shows that the orientation of the scaffold constrains the orientation of added subunits. This does not mean that the scaffold is ‘in control’.
CharlieM,
Actually, there is a much more succinct answer to this attempt to dismiss DNA’s central role: I believe the ‘formative principle’ is DNA. There. Done, and done!
Evolution needs it? There is in fact no current satisfactory explanation for how complex innate behaviours are heritable. It is, for me at least, a fascinating conundrum. As Allan Miller points out the space and materials for packaging heritability of innate behaviour is limlted. Scientists could throw their hands up and assume there is no physical explanation and default to inventing “supernatural” explanations but that would be a retrograde step in the direction of “Intelligent Design” fantasies.
We have a candidate in DNA and we should also consider epigenetic elements in maternal cytoplasm. My money is on DNA.
And we don’t have to start with the most complex examples of innate behaviour. The simplest I know of (sorry to repeat but I think it bears repeating) is the “run and tumble” strategy of flagellate bacteria such as E. coli. A bacterium, with an input of current concentration of, say, glucose, and a memory of a previous concentration, either swims in a straight line or, by reversing flagellum rotation, tumbles over ending up in, most likely some other random direction, swims again in a straight line. This simple strategy keeps the cell in optimum nutrient concentration. And it is a chemical process, albeit rather complex, and tractable to scientific study.
Except he’s not, is he? He’s posting a few OP’s on a low traffic blow that happens to have a few scientists as members.
When Sal gets a paper published that makes it through peer review then perhaps what you say will have some truth to it.
And in any case, Sal is not here to kill the evolutionary nonsense, he’s admitted that he’s here only to find out which of his arguments are easily refuted so he can abandon those to concentrate on the arguments that his target audience can accept.
So you have been played J-Mac, just like all the children being lied to by Sal.
Allan Miller,
Ach, I left myself wide open. Mung joke in 3 … 2 … 1 …
J-mac, thank you for your participation. Something I should point out. What I am mostly attempting to contribute in these sort of technical discussions is giving a more balanced view of the DNA functionality than what is promoted by Larry Moran and Dan Graur and evolutionary biologists like John Avise and Francisco Ayala and the whole gang of them that promote the notion most of the human DNA is junk.
It seems that this crew of “we are junk, and we love being junk” is deeply offended by the work pioneered at the National Institutes of Health and others in the medical research community.
If one were to visit some of the biochemistry classes at the NIH, one would be introduced to a sampling of the 40 or so classes of EXPERIMENTS (versus arm-chair theories of “we are junk and we love being junk” theorists). Here are a sampling of those experiments listed by the ENCODE consortium. Outside of the ENCODE consortium, is now the even bigger RoadmapEpigenomics Consortium. All told, almost a 600 million dollar research inititiative that probably is only the beginning of even more.
Some of the results and consequences of these actual experiments (both ENCODE and beyond) I’ve simply reported here. The FIRRE lncRNA, the HOTAIR lnc RNA, the XIST lincRNA, the Alu A-to-I edited dsRNAs, the microRNAs, the staggering molecular machines associated with these — I just report on.
The 3C, 4C, 5C, 6C and High-C classes of experiments are very important. I may go into why as time goes on, but you got a hint of it in my posting on the Origami Code and the FIRRE lncRNA.
I’ve been disturbed that VJTorley gets a bit too much of an imbalanced view by focusing so much on Larry weblog. VJ came to TSZ to here the other side, and now I’m giving the other side. 🙂
I have found that experimental facts and patience are a much better avenue to truth than the rush to judgement of the “we are junk, and we love being junk” crew.
Except the difference between you and that crew is they publish and open their work to the formal criticisms of others. They then feed those criticisms back into their work, improving it.
You do none of that.
Demonstrate it. Write a paper demonstrating why that crew are wrong.
stcordova,
I think its good stuff. It certainly take a bite out of the “Well, once there was a simple replicator, that got some accidents” crowd.
phoodoo,
Sure, but how do you know it’s the good stuff until people who also have knowledge of the field have gone over his work and pointed out errors?
Presumably because the person saying it has the same agenda as you, you think it’s the good stuff. Plenty of people have pointed out why Sal is wrong or has come to the wrong conclusion, but none of that matters to you does it?
When Sal publishes his work and gets it out there past peer review then perhaps you’ll have a point. But until then it’s just posts on a low traffic blog that mean nothing.
stcordova,
You keep saying this, and one can only keep saying that isn’t true. I honestly couldn’t give a shit what the functional percentage in me or any other organism is. It’s very high in bacteria and fugu. It varies enormously in some genera. Biology is not all about people.
As I have said, it was considered 100% in my uni day. I did not find that offensive. I understand and accept the current arguments that it is substantially less than that. Any idea that one should base one’s assessment on worldview is crass projection.
If people successfully refute those arguments with data or properly addressing the mutational load argument, I will cheerfully change my mind. But that has not happened yet. It is a work in progress at best. This repetitious accusation of unbending dogmatism from the Creationist community is decidedly rich.
OMagain,
Its not only Sal’s work Omagain. Maybe try reading it?
The DNA basis of innate behavior is just an extension of the problem of design.
How do you design something like orb weaving behavior in DNA. One can disrupt the behavior by mutating the DNA, but what are the design principles?
You have evidence for that?
Unless you mean giving them brain damage. Which disrupts every behavior.
How can genes that need to be expressed at the same time get expressed, and done so based on which cell type the genes are in? One way is through transcription factories!
Below is a diagram of a transcription factory from Nature genetics. From this old article:
http://www.nature.com/nrg/journal/v6/n9/full/nrg1673.html
It depicts the emerging concept known as transcription factories.
The reddish bubbles are sections of DNA that are being transcribed. Notice that 4 different sections of DNA are being transcribed simultaneously! And as Rinn demonstrated powerfully with his FIRRE lncRNA discovery, the DNAs could be herded from multiple chromosomes at the same time into the same location by the action of lncRNAs.
The green ribbons are RNAs that are important to the process in each bubble.
Now each of the 213 (or maybe thousands) of cell types create different sets of transcription factories on the fly based on the Origami Code.
What this concentration of reddish bubbles (in the diagram) in one 3D location creates is what is known as a transcription factory.
Transcription factories are described in this Wiki:
https://en.wikipedia.org/wiki/Transcription_factories
The Origami Code illustrates the process of formation of many transcription factories, often simultaneously. The mechanism of formation is now believed to be through the scaffolding, guiding and shepherding of RNAs.
Rinn’s discovery of the FIRRE lncRNA and the Cat’s cradle hypothesis shows how a transcription factory may form between seemingly unrelated genes on separate chromsomes (like X, 2, 17).
Many times for gene expression to work well, it entails genes are expressed in concert together, and many of these genes are on separate chromosomes. FIRRE lncRNA, XIST lncRNAs and several others being researched are involved in enabling the linking of genes on separate chromosomes to be focused into the right location.
What is amazing about this Rube Goldberg mechanism should be obvious. When one pulls DNA from several different chromosomes, it constrains how DNA on the other chromosomes can be accessed or formed into other transcription factories simultaneously. This can’t be done unless the DNA is carefully organized into pretty specific patterns on large scale.
It highlights that DNA sequences can’t be willy nilly laid out on chromosomes and the lncRNAs that coordinate the formation of transcription factories, otherwise these cell-type specific factories wouldn’t form and hence distinct cell-types within distinct tissues and development phases may not even develop!
The amazing thing one can see with Rinn’s FIRRE lncRNA example where genes from 2 and 17 are linked, to form several coordinated transcription factories in a coherent fashion takes a lot of coordination in laying out the DNA, and it must take into account not just one set of factories but the 213 (or maybe thousands) of SETS of factories that are assembled on the fly in 213 (or maybe thousands) of cell types. Cell types are type like liver cells hepatocytes, beta cells in pancreas to make insulin, nerve cells, skin cells, bone cells, blood cell making cells… whatever.
So we see then, the 3D dynamic architecture of DNA is very important, and this puts a design constraint on the DNA sequence. It can’t be willy nilly. The sequences are functional almost by default in their support of the 3D geometry (topology is the more erudite word) of the DNA/chromatin complexes. And to pile one to the importance of DNA sequence in the support of 3D transcription factories, let us not forget DNA sequence is constrained such that it can help wind a certain way around the nucleosome, so there is the constraint that DNA sequences support some sort of curvature and nucleosome positioning (the nucleosome and chromatin code). All these constraints, both in terms of protein coding, transcript function, and 3D topology is what Robert Marks and John Sanford refer to as polyconstraints. They published a paper with Montanyez and Fernandez that shows that Darwinian processes do not construct such polyconstrained structures as a matter of principle.
http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.684.608
PS
[as an aside, before I forget here is a good article on lncRNAs and the brain
http://journal.frontiersin.org/article/10.3389/fgene.2014.00164/full
It’s worth a discussion on its own.]
]
I finally have to respond to this:
Man, you totally don’t understand what is going on, so maybe I’ll set you straight. Larry is valiant defender of “our genomes are 90% junk”. He and a few dwindling numbers are the last Samurai who are defending a viewpoint that is going the way of dinosaurs.
I was merely saluting the last Samurai. I commend him for his valor and determination in a losing cause.
So you might reconsider this before you urinate all over my cordial gestures to Larry in the future. Keep your stuff zipped up the next time.
Larry is likely wrong and definitely hasty to say 90% of the genome is junk., but I bow down in respect for a good scientist and great professor of biochemistry, Larry Moran.
They didn’t publish anything in the peer reviewed scientific literature Sal. This piece of dogshit was from the fake Creationist conference in the rented hall space at Cornell.
You can’t be honest even for a millisecond, can you?
LoL. Robin seems to think it a very bad thing to think like Mung. Careful. 🙂
My God is Big. Really BIG.
That’s just wrong. My God is Small. Really small. The smallest gaps will do quite nicely. The smaller the better.
Darwin’s theory was supposed to give you a designer substitute. So when it comes to evolution, any problem for design is a problem for evolution as well.
The DNA basis of innate behavior is just an extension of the problem of evolution. DNA “accidents” is the answer to everything.
Also, it is completely wrong-headed to think that design principles cannot be discovered in biology.
What’s that? Oh, another argument from fucking analogy. Keep it to yourself, thanks
Moved a comment to Guano. Accusing other participants of dishonesty is against the rules.
On the search for design principles in biological systems
Here’s the full paper
http://wwwuser.cnb.csic.es/~jpoyatos/Publications/EvoSysBio_Ch9JFP.pdf
I have no idea what any of that is supposed to mean to be honest. Apparently the author is not a biologist, he has a PhD in Quantum Computation.
What’s your point anyway?
VJ Torley asked about the Hox13 over expression. From the original paper:
VJ asked:
A trait that induces removal from the population by an average of 3-5% implies it is deleterious as far a reproductive success by definition. Traits that deform individuals in this way do not improve reproductive success.
Before they trumpet that this solves the problem of limb evolution, they should see the effect of the mutation in adult populations. Do these Hox13 freaks (with malformed fins, even if other wise normal in the body plans) attract mates? !!!
If male zebra fish perceive the new Hox13 females like the average guy perceives the hypothetically mutated girl from the Zombie Apocalypse (below), I don’t think the mutation could be considered reproductively advantageous.
The average guy is desperate, Sal.