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.)
Meiosis is a huge problem for blind watchmaker evolution. If one wants to talk about sexual reproduction that needs to be addressed first.
Hold on! 🙂
Epigenetics is often conflated with Larmarkianism and Lysenkoism, as Moran characterizes it solely in terms of germline transmission between generations and totally misses the far more important aspect of somatic cell transmission between a cell (like a stem cell) and its daughter cells.
Epigenetics is also important in repairing DNA in an existing cell when it is broken. Example of the epigenetic complexity in this process is depicted below. That diagram comes from this paper which should give you a different perspective versus Larry’s dismissive view of epigenetics:
http://www.intechopen.com/books/new-research-directions-in-dna-repair/chromatin-remodeling-in-nucleotide-excision-repair-in-mammalian-cells
Unfortunately, most IDists don’t understand epigenetics either!
But it actually is very very important to somatic cell lines. If anyone doubts the importance of epigenetics and the epigenetic pharma market consider these facts:
The NIH and RoadmapEpigenomics projects explore epigenetics and has a 500,000,000 budget. Epigenetic modifications in somatic (not germline) cells are very important to development and gene regulation, and hence add a level of complexity that is staggering. The genome has about 1 gigabyte of information, but the sum total of bytes of networked information in epigenomes in the 100 trillion cells of human body could house:
1,000,000,000,000,000,000,000 bytes
Also the Pharma companies are spending billions on epigenetic therapies, and the FDA has already approved treatments to go to market. Unfortunately, my published discussions of this were a tad watered down in the AM-NAT 2016 conference, but you can access a free draft copy of my writing here that doesn’t have the virus warning:
Larry’s a sharp guy, I like what he writes, but he’s not seeing the other perspectives on the problem epigenetics poses that are beyond transgenerational inheritance between parent and child, but ignores the somatic inheritance from one cell (like a stem cell) to daughter cells — that’s where the big research and pharmaceutical market are, and Larry gives the impression such things are inconsequential, they are not. That’s part of the reason ENCODE believes the genome is 80% functional, the epigenome.
The complexity of the epigenome is staggering in the network of somatic cells. Don’t let Larry get away of framing the issue solely in terms of germline cells, the importance of the epigenome is in somatic cells.
Since you’re talking embryogenesis, you might be interested to see this discussion.
Note the photograph below that show EPIGENETIC changes to the embryo over the course of hours. I learned of this in my graduate Biochemsitry class at the National Institutes of Health (NIH), an institution which Dan Gruar (Larry Moran’s colleague) has a very low opinion of.
But a picture’s worth a thousand words. Before you dismiss epigenetics, look at the picture of epigenetic changes to the embryo!
Oh, yes. New body plans can’t form by means of gradual evolution because Paul Nelson says some necessary mutations are always lethal. So those body plans must have appeared fully formed.and Vincent buys the argument.
OTOH Vincent accepts common descent between species with different body plans but is somehow incapable of connecting the dots and figuring out the absurdity that logically follows from that.
Yeah, yeah, I know I keep repeating myself, sorry about that.
stcordova,
Go on then, how much of this is controlled by anything that doesn’t originate in garden-variety DNA, inherited along with the rest of the genome? Epigenetics is just a modish buzzword. It’s genetics, with DNA as substrate.
Genomes don’t do anything by themselves.
Frankie,
Everything that genomes ‘do’ has its root in a gene, inherited by template copying of DNA (occasionally RNA, ‘gotcha’ fans). Everything. Including polymerases themselves. If you know of an exception, let’s see it.
If you have evidence for your claim, let’s see it. DNA does not copy itself. DNA gets copied along with everything else in the cell.
DNA in a blank cell- just cytoplasm- does nothing
Unknown because glycans are not coded directly by DNAs, but by other glycans. Even supposing descent with modification of DNA, the glycans today may owe their pattern to DNA that no longer exists, hence the heritable characteristics of glycans are no longer strictly based on the genome of the organism it is in ( it could hypothetically be coded in part by DNA of the ancestral genome that no longer existent), same for the proteome/interactome.
I also pointed out experiments in favor of cortical, structural and other non-DNA inheritance mechanisms outside of chromatin modification (aka epigenetics):
But the fundamental intuition that Larry Moran’s implicit vision that 88 megabytes (the fraction of the human genome he thinks is function) of genomic information can create something as complex as a human seems absurd. Seems there must be a lot more information out there than beyond the genes, and the glycans are an example.
What’s the upper limit in FIASCO that 88 megabytes of FIASCO can create?
Great post.
Hold on 🙂
This argument is still alive and kicking. Although Rumracket did write an excellent post it far from refuted that functional protein space is rare in sequence space. The question Rumraket has not been able to answer is why there is variation in how rare the sequences are.
Szotack’s experiment is for ATP binding. His results show that in an 80 AA sequence the odds are 1/10^11.
Is this abundant in nature?
This means I need 100 billion trials starting from a random sequence before I have reasonable chance to bind ATP.
What if I also have to catalyze a reaction?
It is logical that this is not as rare in nature as a more complex function. Axe’s experiment is for binding with another sister protein and then breaking down an antibiotic molecule. This was estimated to be 1/10^77.
Does Axe’s complexity exist in nature? It is just the tip of the iceberg.
How does nature with a trial and error process build a mobility with a 30 protein complex that all need to bind together to perform a specific function?
I once asked you if your genome was randomized. Starting to believe it probably was
stcordova,
And glycans aren’t made by genes? Glycans are replicated independently of the genome?
Nobody doubts this. Nobody has ever doubted this. What else could cause differences among somatic cells? What people doubt, and what Larry Moran dismisses, is that epigenetic inheritance across generations has any significance for evolution or for the differences among species.
Does it really matter? The more interesting and relevant question is the one you raise later:
IOW, how far downstream are HOX genes and are changes in HOX genes sufficient to explain new body plans or only variations on an existing plan?
VJT, have you ever written an OP on what a body plan is? Are there any fans of “it just happened, that’s all” that would like to give it a shot?
stcordova,
But blissfully ignored the ‘grandparents’ problem. Genes are discarded at random, 50% each offspring. What causes ‘epigenetic’ inheritance to assert itself, when there are 2, then 6, then 14, then 30 (…) cytoplasmic ‘experiences’ vying for attention? Mendel neatly solved the dilution problem for genes. Where an epigenetic modification is attached to DNA (methylation, histone), it is discarded in like manner, although there is (very limited) scope for cross-generational effects. There seems no equivalent for ‘cytoplasmic epigenetics’.
I think I see an appendix!
Mung,
I don’t think there are many ‘body plans’. They seem to me to differ mainly at phylum level (which were once ‘species’ with some developmental plasticity that has since become less labile as the phylum itself has diverged). It’s a word that seems bandied around rather freely – every baramin has a ‘body plan’, and you dumb evilutionists can’t explain ’em so they’re different. So you get a goose body plan and a duck body plan, an ostrich body plan, a cassowary body plan …
stcordova,
If we’re lucky, we get a picture and a thousand words!
Allan Miller,
The active form of vitamin d which is mission critical for DNA transcription including the cell cycle process. The small molecule is synthesized in the skin from ultraviolet radiation and then modified in the liver and kidney. The active form binds with the VDR protein as part of the transcription process.
colewd,
Is any part of that processing not under ultimate DNA control? News to me. Obviously the photons don’t come from my DNA. Nor does the sandwich that keeps me typing this drivel. Yeesh. I mean, look at plants. Photons a gogo. Not exceptions.
If all people are going to do is point to photons, or non-DNA electrons or something …
Where is your evidence, Allan? Why do you always ask for others to support their claims and yet you never do?
OK, when and if you ever get the evidence to support that claim please present it. Otherwise no one cares what you think. You think the genetic code isn’t a real code.
Mung,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC299744/
Miracles- that is all you had to say, Allan. Blind and mindless processes just happened to duplicate the HOX genes- do you guys even read the crap you post?
Frankie,
No, some bloke in the sky did it, of course. Sometime. For some reason.
[eta – here are some duplications that occurred in the hagfish. ‘Cos, y’know, God just loves hagfish. ]
It’s always nice to see evos take a loss like a child
Frankie,
Here you go
The term “body plan” refers to the general similarities in development and form and function among members of a particular phylum.
I am merely following general usage in biology. You have decided ‘body plan’ means something else.
You care so little what I think that you tell me off for it on a regular basis. Still, you are correct, I don’t think the genetic code is a ‘true code’. I have my reasons.
Mitochondrial organelle’s are inherited. They serve as templates for future mitochondrial organelle’s. I think (am not sure) these are non-medelian heritable features.
This fact can be leveraged in principle for curing some heritable mitochondrial diseases. Not only is the mtDNA changed, but the entire mitochondria itself. It is an illustration of organelle inheritance.
https://www.theguardian.com/science/2015/feb/02/mitochondrial-transfer-micro-transplant-parliamentary-debate
New epigenetic (aka chromatin modifications) may mostly drift out of the population, but that doesn’t prevent fixation any more than the fact most neutrals don’t get fixed, but one might get fixed.
Also, whatever creates the methylation marks can change, and no one really knows where the data reside that re-print/reset methylation marks per generation, but these marks are nonetheless species specific.
For example:
Obviously humans have different epigenetic marks than other species. We argued over what constitutes “heritable” for epigenetic marks, but well, those marks are different between species, so something got inherited and fixed, that’s for sure.
Frankie,
Evidence for what? I’m asking people to support their claim regarding epigenetics. My claim is that they cannot come up with an epigenetic mechanism that does not root in DNA – an enzyme, an RNA or the control thereof. I cannot ‘support that claim’ by anything other than sitting back and waiting.
stcordova,
They pass through the maternal line. That’s how that particular ‘dilution problem’ is managed. They don’t have to be, of course. But then, one mitochondrion still ends up the mother of all, in pretty short order, much like bacteria in a chemostat.
They are in the 1% of DNA that is different.
Would you agree or disagree that according to your source, within a phylum there can be innumerable body plans?
Allan Miller,
The only form of DNA control is the modification of the molecule in the liver and kidneys by enzymes that are generated from DNA. I think a lot of small molecules fall into this category which are being manufactured by enzyme reactions.
We are a lot more like plants then I thought before doing research in this area 🙂
Oh yea right, the the lack of a naturalistic explanation for the origin of biological information problem, and the functional coherence makes accidental invention fantastically improbable and hence physically impossible problem have been adequately dispelled by a couple of posts on Sandwalk.
Whew, glad we took care of that!
VJ wipes his hands and soldiers on towards the truth. Hooray!
Who says accidents can’t do wonders-its no problem! VJ now you just have to get your new friends to agree to use the word accidents then, because they sure as hell are afraid of that.
And a soundtrack.
The focus seems to be on adaptive radiations. As a layman, I take that to mean diversification within a given body plan.
If different body plans all share a common mechanism for diversification [adaptive radiation] I’d classify it as a miracle.
I mean, what are the odds?
That genomes dictate all
And yet members of the same phylum can have different body plans
Allan, you are asking way too much of blind and mindless processes. How can we test the claim those alleged duplications were accidents, errors or mistakes?
And how can that produce HOX genes in the first place?
That’s false. That would imply Larry thinks the only fraction of the genome that is functional is strict protein-coding sequence (which amounts to roughly 3% of 3.2 Gb = 88 Mb), and that everything else is nonfunctional. He has been rather open about saying he thinks the correct number is more around 10% of the genome.
He obviously includes transcription factor binding areas, telomeres, centromeres, enhancers, promoters, many types of functional RNA’s (including ribosomal and various translational and regulatory RNAs) and so on and so forth, none of which is strictly coding for proteins.
Considering how much time Larry spends trying to debunk and fight the strawman and mistaken view, that “geneticists used to think only protein coding DNA was functional”, your accusation that Larry himself is guilty of this mistake is scandalous.
You’re math and Shannon information understanding is a bit shaky and hence you’re attacking a claim I’m not making.
The Shannon capacity of each nucleotide position is 2 bits, that is based on the for possible states (Adenine, Cytosine, Guanine, Thymine) of each nucleotide position. So we take log base 2 of 4 states:
log2 (4) = 2 bits
so 3.3 giga bases (you used 3.2, that’s ok) = 6.6 Giga bits
10% * 6.6 Giba Bits = 660,000,000 bits = 660 Mega bits
A byte = 8 bits therefore
660 Mega bits = 660 Mega bits * (1 Byte/ 8 Bits) = (660 Mega / 8 ) byte
= 82.5 megabytes.
So actually I was even being too generous by saying 88 megabytes. I probably was remembering another calculation, but using your figure of 10% and even giving you a little extra (3.3 Gb instead of your 3.2), I got even LESS than 88 Megabytes, but 82.3!
I said:
I did not say mega bases (Mb) , nor mega base pairs (Mb) , nor mega bits (Mb)!
But IT folks will recognize, 82.5 megabytes (Mb) that is not a lot of information. I’ll cut you some slack because the acronym Mb is ambiguous since it has 4 possible interpretations!!!!
FYI:
https://en.wikipedia.org/wiki/Byte
You said:
Your accusation is rooted in not understanding what I said, namely confusing bytes with bits, bases with Shannon bits, etc. My main mistake was being too generous. So I revise my figure from 88 to 82.5 thanks to you. So Larry has even less room to work with, now.
There, how promising do you think most engineers would feel building something as complex as a human with 82.5 megabytes?
I’m an IT folk. That is a lot of information. Try writing 82.5 Mb of source code.
The issue is the total memory needed. Compiled code, plus the memory needed to run the Operating System, the compilers, the executable, in the case of Java, the Java Virtual Machine — it’s big.
But, do you think with even 82 Mb of source code you could create a self-replicating 3D printer that has the capacity to smell and remember smells, to see and remember sights (an eye can almost detect a single photon), to hear and remember sounds (not to mention carrying out the equivalent of Fast Fourier Transforms and then some), to taste and remember tastes, to touch and remember touch, to balance, to coordinate, to walk (try building robot that can walk), to digest nutrients and build and develop…..all this happening from building blocks at the nano-scale where Brownian motion and other disorganizing mechanism are constantly requiring self-repairing mechanisms.
Oh, that’s the other thing, can your source code fix it self-when it is broken due to a hardware failure? Above I showed this picture of DNA excision repair. How do you ensure such breaks are properly fixed? I’ll give you an even more complex diagram of DNA repair involving epigenetic factors. Can you build anything like this?
This only one of the EPI-genetic pathways involved in genetic repair. So Larry is so dismissive of epigenetics, and yet is is only one miniscule aspect of what and epigenetic system does, in this case it is repairing a genetic system.
I recommend just looking at the picture, but if you want to get taste for the complexity of just this one epigenetic pathway, read for yourself the description of what is described in the diagram below:
http://jcs.biologists.org/content/125/2/249
You’d think by now the IDiots would have realized that the “complexity = design” argument has failed as thoroughly as any argument can fail. But if they had any reasoning skills I suppose they wouldn’t be IDiots.
I’ve seen it. The first time I was working on a project being run by one of the big consulting firms. They had a blowout party when they went over the 1 million lines of code mark. Those of us who knew better sat in the corner and held a quiet wake.
we’re 3 mos away from Paul Nelson Day.
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blockquote cite=”comment-161011″>
Adapa: You’d think by now the IDiots would have realized that the “complexity = design” argument has failed as thoroughly as any argument can fail.But if they had any reasoning skills I suppose they wouldn’t be IDiots.
Against the rules according to Alan. Alan made this very clear. How did he put it:
No, I mean against the rules if a theist did it.
So in that case, just want to give Adapas comment a thumbs up! Great stuff!
I will highlight Larry’s rhetorical trick of dismissing epigenetics by saying, “methylation is trivial” or saying “Histone modifications are never inherited”. There’s a lot of equivocation going on.
But first, below is a picture of the epigenetic research market showing money invested (in millions). It is taken from this report:
All this to point out, Larry is perpetuating a distortions about epigenetics that is unfortunately echoed by some ID outlets (like Uncommon Descent).
The NIH has a 300 million dollar RoadmapEpigenomics research project. I wonder if Larry would like to tell them their work is no big deal, that most of what they do is generating noise. Would they take kindly to Larry saying of their work,
“methylation is trivial”.
Larry equivocates the issue. Yeah, no big deal to add a methyl group to a cytosine DNA randomly, but the issue is adding the methyl or removing it at the right time and the right place! The effects are lethal or really really bad if that’s not done. Look at the lighted dots changing in the diagram of this comment:
Those are large scale changes in the methylations happening on the embryo in a matter of hours. It is a picture of changes of the Random-Access Memory (RAM) of the cell implemented on the methylation marks. My detractors balked at my characterization of methylation marks as RAM, until I showed them a passage from the 2013 Stem Cells handbook. Bwahaha! The cells implement a networked topology of 100 trillion cells with a sum total of sextillion bits or so of methylation implemented Random Access Memory.
But Larry Says, “methylation is trivial”. Yeah right Larry. You’re just equivocating what people mean by the complexity of methylation. Larry is talking about adding methyl groups to a random cytosine DNA, the epigenetic community is talking about having them added in the right place at the right time. That’s an equivocation. That’s like saying DNA is trivial because it’s just adding a nitrogenous base to a sugar-phosphate back bone. 😯
Naughty naughty, Larry. But you’re words are now going through the turnpike of truth (to paraphrase Rush Limbaugh).
Larry says, “Histone modifications are never inherited”. there is an equivocation there. Larry speaks of the ability to read a histone and then duplicate it transgenerationally in the germline. Basically a copy-and-paste operation. DNA duplication is copy-and-paste (so to speak).
But the data for creating histone modifications in the right place and at the right time is more than just copy-and-past reading! For example, I called him out on it on his blog regarding the HOTAIR linc/lnc RNA and the polycomb repression complex (PRC2) methyl modifications on histone 3 Lysine 27 that induces skin cells at the soles of the feet to be different than skin cells at the eyelids. Carl Zimmer gives a nice layman explanation of this INHERITED histone modification.
By inherited, I don’t mean copy-and-paste (like DNA), but meaning the modification is present in parent and child, and we don’t yet know how or why.
You see, the heritabiltiy of histone modifications is a bit more subtle than copy-and-paste but involves a cascade of events. If by “Histone modifications are never inherited” one means “no copy-and-paste inheritance (like DNA)”, then Larry is right, but if one means “no inheritance of mechanisms that create the same histone modifications over and over again between generations” — HECK NO! A child has the same Histone 3, Lysine 27 methylation 3 patterns as hisparents. So something is inherited as far as histone states, not but not through copy-and-paste (which is the way DNAs are inherited). We actually don’t know how those histone modifications systems are inherited! By histone modification systems, I mean like some of those shown for DNA repair, the HOTAIR-to-PRC2 system, and who knows what else. Naughty, naughtly Larry. But your words are now going through the turnpike of truth. But I credit you with some clever equivocations.
Finally, look at some of the publications the NIH RoadmapEpigenomics consortium alone (not to mention other institutions) put out (in some very fine peer-reviewed journal). I wonder how they would react to Larry characterizing their analysis of methylation as “trivial”. He can put up his analysis along with theirs in the same journals:
http://www.roadmapepigenomics.org/publications/
🙂
You have to be an idiot to think ID makes the argument that “complexity = design”, especially seeing that IDists are OK with nature producing complexity.