Early embryonic mutations: a problem for evolution?

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.)

585 thoughts on “Early embryonic mutations: a problem for evolution?

  1. Rumraket: 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.

    What does it mean to say that something is the result of an evolutionary process? Isn’t everything the result of an evolutionary process?

  2. Rumraket,

    Is Sal perhaps displaying a bit of the creationist distinction between experimental science (good, except when it isn’t) and historical science (bad, except when it isn’t, and that isn’t often)?

  3. Mung: What does it mean to say that something is the result of an evolutionary process? Isn’t everything the result of an evolutionary process?

    Evolutionary processes have clear entailments. Not everything conceivable can be the result of them, but the evidence confirms everything in existence was.

  4. Frankie: I love how the Patrick just blindly accepts what others have to say about IDists.

    Due to a lack or critical thinking skills I’m inferring child abuse.

    He finds a treaty with the Mohammedans from 1797 that says ““the Government of the United States of America is not, in any sense, founded on the Christian religion” and that’s all it takes, sez he, to contradict my claim that the concepts underlying the Declaration of Independence and the Constitution of the United States are Christian/Biblical/Religious/Creationist concepts.

    That one statement from one treaty contradicts all history. LoL. And Patrick wonders how Dembski can say different things to different audiences.

  5. Rumraket: Who’s actually impressed by this galloping technobabble?

    Not I.

    [ETA: Not that it’s not impressive. It is. LoL. I’m just immune.]

  6. Allan Miller: Better yet one who thinks there is a mysterious undetectable ‘field’ surrounding biological molecules as a way out of the wholly imaginary ‘DNA problem’.

    Did he says the fields were undetectable?

  7. Mung,

    Did he says the fields were undetectable?

    No, I did. Maybe he has an orgone accumulator or summink, I don’t know. If it’s got lots of whirly wires on it, I would of course totally change my tune.

  8. Allan Miller: You’ve just imported the entirety of a class to ‘functional’ based on a few instances. It doesn’t work like that, as I said.

    So someone came up with this idea of “junk” DNA. Then people started putting things into this category of “junk DNA.”

    Did they test every instance for function, or did they make generalizations? I’m thinking they did it the way that you say it doesn’t work that way. But what the hell do I know.

    How did they determine how many presumably non functional sequences they ought to actually test before they reached a conclusion? Do you think they even went that far?

  9. dazz: Sal’s strategy consists in finding some instance of function to then affirm that the null hypothesis must be function, because showing something in particular has no function is a lot harder.

    Why wouldn’t function be the null hypothesis? Don’t organisms exist with little to no “junk” DNA?

  10. Mung,

    So someone came up with this idea of “junk” DNA. Then people started putting things into this category of “junk DNA.”

    Did they test every instance for function, or did they make generalizations? I’m thinking they did it the way that you say it doesn’t work that way. But what the hell do I know.

    If a transposon, which produces proteins that enable it to transpose, does not have a functional version of the proteins, then it cannot transpose. A large fraction of the genome consists of such fragments – they have a tendency to break on landing: the original sequence can produce the protein, the copy cannot. How many versions of these sequences should they test before they can determine it’s junk? They can be shown to be inactive, en masse.

    Now, contrariwise, people are insisting that there are some functional versions of these sequences, because part of them has come to lodge in genes. And sure, the ones lodged in genes, you can have. That’s a few hundred, a few thousand maybe. The rest still can’t transpose. Their function is obviously not the same function as that which lodged in genes (if that is function), because they are neither lodged in genes, nor can they get there, because they are broken – they cannot transpose to a gene.

    So, each one proposed to be functional needs to be shown to be so; the reverse is not true, because they have been shown to be ‘broken’. Whatever function they have, it cannot be related to transposition (because they can’t do it) nor donation of sequence to gene or promoter/repressor (because they are not in gene/promoter/repressor).

  11. Mung,

    Why wouldn’t function be the null hypothesis? Don’t organisms exist with little to no “junk” DNA?

    Sure. In them, there is no need to look for exotic fractal gobbledeomes. They are packed with coding sequence, and very little of the ‘intergenic’ stuff that people are inisisting is packed with function (and yet which these other organisms can easily do without).

  12. Mung: Why wouldn’t function be the null hypothesis? Don’t organisms exist with little to no “junk” DNA?

    You’re so fucking amazing. The answer I would give you was right there in the very post of mine you quoted, only that… wait for it.. YOU IGNORED IT! AGAIN!

  13. Mung, I was obviously referring to human jDNA (or onion jDNA for that matter). There’s POSITIVE evidence for a 90% junk in humans, a lot more in onions and none in pufferfish

  14. Allan Miller:
    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 anyone is arguing against the importance of DNA is just a figment of your imagination. Just so that it is clear in your head I will tell you that IMO DNA is central.

    Do you understand that I am sure that the DNA is the means by which my body is built up. I’m going to embark on a fantasy of my imagination now and ask you to picture that I have taken up body building. Through an act of will I do some weight training, I stick to a suitable diet and I actually do begin to put on muscle.

    If it were not for the central role of DNA in the process of converting my food intake into muscle this could not happen. But this was all instigated by my thinking and my will, not by my DNA.

    From Getting Over the Code Delusion by Stephen L. Talbott:

    Cells of the mature heart and brain, then, have inherited entirely different destinies, but the difference in those destinies was not written in their DNA sequences, which remain identical in both organs. If we were stuck in the “chimp equals human” mindset, we would have to say that the brain is the same as the heart.

    So what’s going on? Let me summarize it this way. The modest number of human genes compared to the gene counts of much simpler organisms gives us good reason to abandon catchphrases such as “DNA is the Book of Life”. Genes are no more the defining feature of human life than are the proteins that maintain and employ our DNA with such profound effectiveness, or the membranes that so intricately and adaptively structure all the activities of our cells.
    Second, the huge amount of non-protein-coding (“junk”) DNA in the human genome gives us good reason to abandon the idea that coding for proteins is the be-all and end-all of DNA. Molecular biologists are in fact rapidly discovering that noncoding sequences play crucial roles in the regulation of gene expression. These sequences — which are never absolutely determinative, and which by themselves can do nothing — offer countless points of entry for the larger cellular environment to “decide” how to employ its DNA.
    In other words, the current exploration of the expansive, noncoding portion of our genome encourages us to turn from DNA as the explainer of the organism to DNA as a resource the organism puts to its own use. This already suggests an approach to the third problem. If we ask, “How is it possible for an unchanging complex to explain an ordered developmental stream?” the answer is, “It isn’t possible”. It’s obvious enough that things cannot by themselves explain processes. And we don’t need them to. We need to look to the organism itself as a living activity for an explanation of the different uses to which its DNA is put; the DNA doesn’t explain the organism.
    What’s demanded of us is a more living understanding. It is not only that DNA by itself is inadequate to regulate its own genes. What we are finding is that at the molecular level the organism is so dynamic, so densely woven and multidirectional in its causes and effects, that it cannot be explicated as living process through any strictly local investigations. When it begins to appear that “everything does everything to everything” (Dumont and Maenhaut 2001), the search for “regulatory control” necessarily leads to the unified and irreducible functioning of the cell and organism as a whole.

    Long ago when it was thought that one stretch of consecutive DNA coded for one protein and the growth of a body was a relatively simple affair, I could see how people thought that DNA was the master controller of the organism.

    But I can’t see any excuse for thinking like that today with the knowledge that is available to us.

  15. CharlieM,

    Urk. I don’t know who Stephen L. Talbott is, but he repeats one of the common misconceptions of people who don’t know the subject: that science either does or used to equate “non-coding” with “junk”.

    Further, everyone agrees that epigenetic inheritance is crucial in determining cell fate within organisms. That has nothing to do with inheritance over many generations. And it also has nothing to do with imagining that junk DNA isn’t junk.

    Certainly DNA doesn’t build bodies. Development and metabolism are complex interactions among the genome, all sorts of molecules inside the cell, and various external stimuli. But the fact remains that differences among species result from differences in DNA sequences and nothing else.

  16. Mung: You noticed! Are you doing anything Friday night?

    Sorry, I’m thrusting god next Friday. Can you make it on Sunday?

  17. Junk is a null hypothesis that can be experimentally falsified. There’s this publication that gives a brief history of the concept and discusses why keeping junk as a null hypothesis is a good idea:

    Non-coding RNA: what is functional and what is junk?
    Alexander F. Palazzo and Eliza S. Lee

    Abstract
    The genomes of large multicellular eukaryotes are mostly comprised of non-protein coding DNA. Although there has been much agreement that a small fraction of these genomes has important biological functions, there has been much debate as to whether the rest contributes to development and/or homeostasis. Much of the speculation has centered on the genomic regions that are transcribed into RNA at some low level. Unfortunately these RNAs have been arbitrarily assigned various names, such as “intergenic RNA,” “long non-coding RNAs” etc., which have led to some confusion in the field. Many researchers believe that these transcripts represent a vast, unchartered world of functional non-coding RNAs (ncRNAs), simply because they exist. However, there are reasons to question this Panglossian view because it ignores our current understanding of how evolution shapes eukaryotic genomes and how the gene expression machinery works in eukaryotic cells. Although there are undoubtedly many more functional ncRNAs yet to be discovered and characterized, it is also likely that many of these transcripts are simply junk. Here, we discuss how to determine whether any given ncRNA has a function. Importantly, we advocate that in the absence of any such data, the appropriate null hypothesis is that the RNA in question is junk.

    From the introduction:

    In this article we explain several concepts that researchers must keep in mind when evaluating whether a given ncRNA has a function at the organismal level. Importantly, the presence of low abundant non-functional transcripts is entirely consistent with our current understanding of how eukaryotic gene expression works and how the eukaryotic genome is shaped by evolution. With this in mind, researchers should take the approach that an uncharacterized non-coding RNA likely has no function, unless proven otherwise. This is the null hypothesis. If a given ncRNA has supplementary attributes that would not be expected to be found in junk RNA, then this would provide some evidence that this transcript may be functional.

    All of the objections non-junk-advocates bring up are also addressed, such as the suggestion that just because a transcript is expressed at a low level (or at a low level in most cell-types), it can still be functional if it is involved in regulation (by gene-silencing) and so on. Overall it’s a nice balanced discussion.

  18. Mung: Why wouldn’t function be the null hypothesis?

    Because it would be almost impossible to falsify. You could always just reason ad-hoc that there’s some putative function in some obscure situation you just haven’t discovered yet.

    The null hypothesis should be falsifiable. If your null is that it’s junk, in principle it takes a single observation to falsify the null. Having junk as the null doesn’t in any way indicate you shouldn’t test it.

  19. CharlieM,

    That anyone is arguing against the importance of DNA is just a figment of your imagination. Just so that it is clear in your head I will tell you that IMO DNA is central.

    OK, I’ll strike you off the list of people who are arguing against ‘gene centrism’. The remainder, though … am I really just imagining it? Better lie down, I don’t know what to think any more.

  20. Ah, DNA is central but not the whole story. Heh, I never knew that. I thought it was DNA -} organism, and that was pretty much it. Bit like playing the flute, you kind of blow and wiggle your fingers.

  21. John Harshman: But the fact remains that differences among species result from differences in DNA sequences and nothing else.

    There isn’t any evidence or data that says the differences between chimps and humans result from the differences in their DNA. The differences between humans may result from the differences ion DNA

  22. newton:

    The conclusion that his admitted behavior “teaching” kids constitutes child abuse is separate and much more serious than that.

    Right,it belonged in Noyau as well. At the minimum you should have been clearer about the nature and relevance of the abuse.

    I think I’ve been very clear about what Sal admitted to doing and how it constitutes child abuse. I’ve repeatedly included links to his comments describing his behavior.

    I’m fine continuing this in Noyau. I’m not fine with letting Sal get away without being called on his vile behavior.

    If Sal explanation is correct( I vaguely recall Sal saying something different which became the genesis of the charge) using child abuse in that context diminishes by overuse the abhorrent nature of the action. In my opinion.

    I consider what Sal has done to be abhorrent and I’ve explained why.

  23. Patrick: I consider what Sal has done to be abhorrent and I’ve explained why.

    I consider what evos are doing to be abhorrent and I have explained why.

  24. stcordova to Rumraket: What you don’t like that I’m pounding most every class of RNA that Larry declared as junk?

    The only one I really have problems with is ERVs.He wins the day on ERVs, so far.

    I don’t know if you know about this recent research nor how easily available the original paper is, but this link from Science Daily looks interesting:
    Viruses in genome important for our brain

    If it turns out that they are able to influence the production of proteins, this will provide us with a huge new source of information about the human brain,” says Johan Jakobsson.

    And this is precisely what the researchers discovered. They have determined that several thousands of the retroviruses that have established themselves in our genome may serve as “docking platforms” for a protein called TRIM28. This protein has the ability to “switch off” not only viruses but also the standard genes adjacent to them in the DNA helix, allowing the presence of ERV to affect gene expression.

    You continue:

    stcordova
    Charlie M, being involved in missile guidance engineering might actually recognized the terms and feedback loops from electrical engineering.

    I may have occasionally spoken about guided missiles in the odd post, but I am not involved in missile engineering. Fixed wing aircraft and helicopters yes, missiles no.

    And my area is mechanical rather than electrical. But obviously feedback is very important and is ever increasingly being made use of in aircraft control and monitoring systems. Over the decades I have been working on aircraft I have seen massive design improvements in this area. In the early days feedback involved much use of springs, levers, bellcranks and the like. (think of the governors that Dawkins liked to write about). All things that tend to wear and break with constant use. Today computers and electronics have taken over. These are designed by very clever people but they come no where near the complex intricacy of living systems.

    Human designed machines begin crude and improve through trial and error and improving technical knowledge. Living organisms are not like that. From the relatively simple prokaryote to the most complex eukaryote they are all extremely capable of surviving in their natural environment.

    Here is an example of how the body uses the piezoelectric effect, something human designers have only just begun in recent decades to widely use in various industries.

    Bone becomes stronger when subjected to mechanical stress, such as walking, running, weight-lifting, or hard physical labor. When under stress, bone tissue deposits more of the mineral salts that lend strength to bone. When the same stress is removed, bone-resorbing cells (called osteoclasts) go to work and tear down the unnecessary bone. This is why a bone seems to shrink in size when it has been in a cast for some time.

    Why bones thicken during exercise is quite interesting. Evidently, stress on bone causes the calcium phosphate crystals to produce tiny currents of electricity. This is referred to as the piezoelectric effect. This tiny amount of electricity stimulates bone-building cells (osteoblasts) to go to work, and bones become thicker, particularly in the areas receiving stress.

    Biomimicry is a growing field, and many things which have been invented without consulting nature have been found to have been used by nature all along.

  25. Allan Miller to Sal: Of course. Don’t ask a biologist, ask an engineer. Better yet one who thinks there is a mysterious undetectable ‘field’ surrounding biological molecules

    You do realise there are detectable fields around living matter?

  26. CharlieM,

    You do realise there are detectable fields around living matter?

    Of course I do. It’s the undetectable ones I’m having trouble assimilating.

  27. Yes, he has admitted to abusing children …

    A lie.

    He has admitted to behavior that constitutes child abuse. No lie.

    What you are encouraging is the sanction of child abuse.

    A lie.

    You have yet to address the behavior that Sal admits to, but you really don’t like it being characterized as child abuse. Your concern so far is all about Sal and not about the kids who’s trust he’s been violating. Basically it looks like you just don’t want your co-religionist called out on his reprehensible behavior. That’s sanctioning it.

    No lie.

  28. Patrick: He has admitted to behavior that constitutes child abuse.

    That is your opinion. And if your opinion means something then the same can be said of teachers pushing evolutionism.

    So if Patrick wants to say Sal is a child abuser the same goes for evolutionists and for the same reasons.

  29. Patrick: I’m fine continuing this in Noyau.

    An admission of guilt. An admission of actual wrongdoing. An admission the entire discussion belongs in Guano. You’re not as hopeless as I thought.

    Sure, let’s take it to Noyau. You can lead off your first post there by linking to where you first accused Salvador of child abuse and of being an admitted child abuser in Noyau. Accusations made outside of Noyau don’t count.

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