Epigenetics Rules!

_{January 1, 2016

Intelligent Design}

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New news summary out at Phys.Org about ant colonies and their castes. Seems as if this is all being controlled via epigenetic means.

This is not good news if you’re a population geneticist: you know, phenotype changes because of changed allele frequencies (unless, of course, it doesn’t; and then you call it “phenotypic plasticity.” There’s nothing in life that a label can’t explain!!). Well, I guess not.

A snippet:

In the new findings, an interdisciplinary research team led by senior author Shelley Berger, PhD, from the Perelman School of Medicine at the University of Pennsylvania, in collaboration with teams led by Juergen Liebig from Arizona State University and Danny Reinberg from New York University, found that caste-specific foraging behavior can be directly altered, by changing the balance of epigenetic chemicals called acetyl groups attached to histone protein complexes, around which DNA strands are wrapped in a cell nucleus. . . .

“The results suggest that behavioral malleability in ants, and likely other animals, may be regulated in an epigenetic manner via histone modification,” said lead author Daniel F. Simola, PhD, a postdoctoral researcher in the Penn Department of Cell and Developmental Biology. Simola is co-lead author with Riley Graham, a doctoral student in the Berger lab.

Merry Christmas and Happy New Year to all!

Comments

I will certainly admit to struggling to understand what you have said. I don't think I misstated what you said, just put it in context of your earlier comments. Yes, that means reading looking back at those comments, and trying to make sense of them in the light of the next round.
... but because of the rise of epigenetics and directed mutations. Evidence keeps mounting that organisms are capable of such things
People here keep saying this about directed mutation. I'm waiting for the actual evidence.wd400_{October 27, 2016
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It is our opinion that I have made mistakes. And you've formed this opinion by misunderstanding what I have said. Even when I've bothered to clarify my comments, you don't seem to understand the easily understood clarification. You seem keen on feeling I've made a mistake. Thank you for at least tacitly admitting you misstated what I had said. Isn't it strange that this discussion is entered into after an 9 month gap, and you belabor something I wrote 9 months ago as compared to something I wrote 9 days ago. And then end up being wrong. The comments on mutation rates had to do, specifically with the L-D paper, which should be revisited. But not just because of the variable mutation rates, but because of the rise of epigenetics and directed mutations, a la NGE. Evidence keeps mounting that organisms are capable of such things, as well as not only HGT, but LGT. This points in the direction of what you call "evolutionary bioology" needing to be re-imagined. And, of course, they'll be doing that shortly; and, in your neck of the woods.PaV_{October 27, 2016
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Honestly, I can't see the point in engaging with someone who keen to twist and turn to defend their mistakes. Yes, you brought up the idea of a "remnant" from a previous envrionment driving adaptation prior to my mentioning the LD experiemnt (and other "fluctiatoin tests") demonstrates that adapation can happen without such an event. The problem is that you then claimed this was (a) obvious and (b) not a problem for your hypothesis. (and also that i didn't undertsand the LD test, and quite a lot of other stuff about directed mutation). As I say, I think you have to chose one. As to this post. Mutation rates certainly vary according to environment. It's not clear whether this is itself an adaptive response, or just slopiness induced by stress. It's not very relevant to this discussion though, since high mutation rates make many non-adaptive alleles and a few adaptive ones. It would certainly be interesting if cells could produce adaptive mutations on demand. You keep citing papers from the 1980s and 1990s that suggested this might be possible. Do you not wonder why there are so few recent papers on this?wd400_{October 26, 2016
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wd400:
I’m afraid you have to chose one, PaV. It’s either “simply obvious” that a clone produces a mutation that is the basis of adaption in the LD experiment, or (as you first said, then disavowed (?) then came back to ) it’s some remnant of an earlier population.
This is what I actually wrote:
We’re not arguing here about whether a clone produced a mutation or not—that is simply obvious–we’re arguing about whether or not the mutation was ‘random’ or not. You’ve either missed the point, or chosen to miss the point.
You'll notice that I didn't say " [a mutation] that is the basis of adaptation (sic) in the LD experiment." Please read things more carefully, and more careful in interpreting what I've said. As to the "remnant," if you were more careful in your reading, you would have noticed that what I was writing about at that point had no reference whatsoever with the Luria-Delbruck experiment. It was you who brought that up in reaction to my remark. When I mentioned "remnants" it was in reference to the logical development of lac operon thinking. You're not being fair to me when you miscontrue the context within which I make a comment. With this said, you then go over the top:
The latter has the problem of being disproved by the LD experiment (an not only because that experiment does involve a single-cell culture, the small number of cells wiki is talking about is the very small sample taken from that culture to perform the tests).
I was arguing for NGE. That argument, not your mischaracterization of it, still stands: Let me restate some things I said above:
First, to frame what is going on here, and what is at stake: Barry Hall: 1988:————-“Adaptive Evolution That Requires Multiple Spontaneous Mutations. I. Mutations Involving an Insertion Sequence”
As a result, we discuss mutation rates as though they were constants, generally related to cell division, that reflect only the properties that are inherent in the genome of the cell. We (896 B. G. Hall) have ignored the possibility that mutation rates might be highly variable and subject, like other cellular processes, to environmental modulation. These results suggest that spontaneous mutation is a more complex process than we have believed, that mutation rates are not biological constants, and that probabilities of mutation are modulated by normally encountered environmental factors.
Followed by:
Now, as to your specific point:…………………………………. Lenski, Slatkin, Ayala PNAS 1989 Mutation and selection in bacterial populations:
Alternatives to the hypothesis of directed mutation Bacterial populations have served as model systems for studying evolutionary processes ever since the classic experiments of Luria and Delbruck, which demonstrated the occurrence of mutations prior to selection for the traits they conferred. However, several authors have recently presented experiments suggesting that bacteria may have mechanisms for directing which mutations occur, such that the rate of adaptive mutations is enhanced. We do not reject outright the potential for selection acting on molecular variation within cells to produce changes in gene frequency. Rather, we argue that any plausible hypothesis to account for the types of observation reported by Cairns et al. (3), Hall (4), and Shapiro (5) must distinguish between the generation of variation and selection, at whatever levels of biological organization. Cairns et al. (ref. 3, p. 145) assert that directed mutation in bacteria (if it is demonstrated to exist) “could, in effect, provide a mechanism for the inheritance of acquired characteristics.”
The whole idea of varying mutations rates in response to environmental cues was not considered by L-D. From Luria & Delbruck:
“The essential condition for the occurrence of the peculiar distribution studied in the theoretical part of this paper is the following: the initial number of bacteria in a culture must be so small that the number of mutations which occur during the first division cycle of the bacteria is a small number. This will always be true, however great the mutation rate, if one studies cultures containing initially a small number of organisms.”
Maybe it's time to revisit all of this? Let me put it another way: do you think James Shapiro isn't aware of the Luria-Delbruck experiment? He just doesn't think it's binding. You do. All the material I've written, and that you choose to ignore: it's amazing. When it comes to Podacarus sicula, yes, you've state that you don't know how this "trait" arose. (Of course it's not a "trait" but a series of "traits".) Your use of the singular already presages your view of what happened. You want to find a "standing" mutation, and do all the necessary genetic work to find it. (you see, a "series" of standing mutations would be too improbable) OTOH, I cut through all the nonsense, concluded that it was an environmentally caused event, and suggested what type of experiment would prove this. As I stated above, the experimental work was done, and I was proven completely right. None of this makes much of an impression on you. But, it should.PaV_{October 26, 2016
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I'm afraid you have to chose one, PaV. It's either "simply obvious" that a clone produces a mutation that is the basis of adaption in the LD experiment, or (as you first said, then disavowed (?) then came back to ) it's some remnant of an earler population. The latter has the problem of being disproved by the LD experiment (an not only because that experiment does involve a single-cell culture, the small number of cells wiki is talking about is the very small sample taken from that culture to perform the tests).wd400_{October 26, 2016
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BA77: I missed that article by Behe. Thanks. The results of Minnich's experiment are not, of course, surprising. The thought that occurs is this: Darwinists think that 'genes' determine the 'nature' of a thing, when, in fact, it is the 'nature' of a thing that determines how, when, where, and how much a gene functions. It's this 'gene-centric' view that is so wrong, and which allows us to get back to the 'nature' of things when we abandon it. Then, the preserverance of species---which the fossil record demonstrates over and over again---and its nature, begin to assume an importance, something that Darwinism has decimated. (I.e., the 'limitless' plasticity of organisms)PaV_{October 26, 2016
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BA77: Liked everything you posted. wd400 simply 'pigeon-holes' everything he runs into using population genetics to provide the various compartments. Well, if that is the way you were trained, and you've studied it diligently for years and years, who's going to give in to the 'upstarts' (that's us at UD). While I understand the human dimensions of this, it ends up hindering the true progress of science. But how do you get around such a thing? We humans tend to justify who we are and who we think we are. But, as you say, it does lead to "confirmation bias."PaV_{October 26, 2016
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PaV, this article from 2010, which I re-read yesterday, may be of interest to you:
Genome-wide analysis of a long-term evolution experiment with Drosophila - 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments." http://www.homepages.ed.ac.uk/aspiliop//2010_2011/Burke%20et%20al%202010.pdf UCI scientists decode genomes of sexually precocious fruit flies - September 16, 2010 Excerpt: For decades, most researchers have assumed that sexual species evolve the same way single-cell bacteria do: A genetic mutation sweeps through a population and quickly becomes “fixated” on a particular portion of DNA. But the UCI work shows that when sex is involved, it’s far more complicated. “This research really upends the dominant paradigm about how species evolve,” said ecology & evolutionary biology professor Anthony Long, the primary investigator. Based on that flawed paradigm, Rose noted, drugs have been developed to treat diabetes, heart disease and other maladies, some with serious side effects. He said those side effects probably occur because researchers were targeting single genes, rather than the hundreds of possible gene groups like those Burke found in the flies. https://news.uci.edu/press-releases/uci-scientists-decode-genomes-of-sexually-precocious-fruit-flies/
Of related note to directed vs random mutations, I don't know if you have seen this yet PaV but Lenski's infamous Citrate example was debunked by Minnich:
Rapid Evolution of Citrate Utilization by Escherichia coli by Direct Selection Requires citT and dctA. - Minnich - Feb. 2016 The isolation of aerobic citrate-utilizing Escherichia coli (Cit(+)) in long-term evolution experiments (LTEE) has been termed a rare, innovative, presumptive speciation event. We hypothesized that direct selection would rapidly yield the same class of E. coli Cit(+) mutants and follow the same genetic trajectory: potentiation, actualization, and refinement. This hypothesis was tested,,, Potentiation/actualization mutations occurred within as few as 12 generations, and refinement mutations occurred within 100 generations.,,, E. coli cannot use citrate aerobically. Long-term evolution experiments (LTEE) performed by Blount et al. (Z. D. Blount, J. E. Barrick, C. J. Davidson, and R. E. Lenski, Nature 489:513-518, 2012, http://dx.doi.org/10.1038/nature11514 ) found a single aerobic, citrate-utilizing E. coli strain after 33,000 generations (15 years). This was interpreted as a speciation event. Here we show why it probably was not a speciation event. Using similar media, 46 independent citrate-utilizing mutants were isolated in as few as 12 to 100 generations. Genomic DNA sequencing revealed an amplification of the citT and dctA loci and DNA rearrangements to capture a promoter to express CitT, aerobically. These are members of the same class of mutations identified by the LTEE. We conclude that the rarity of the LTEE mutant was an artifact of the experimental conditions and not a unique evolutionary event. No new genetic information (novel gene function) evolved. http://www.ncbi.nlm.nih.gov/pubmed/26833416 Richard Lenski and Citrate Hype -- Now Deflated - Michael Behe - May 12, 2016 Excerpt: ,,, for more than 25 years Lenski's lab has continuously grown a dozen lines of the bacterium E. coli in small culture flasks, letting them replicate for six or seven generations per day and then transferring a portion to fresh flasks for another round of growth. The carefully monitored cells have now gone through more than 60,000 generations, which is equivalent to over a million years for a large animal such as humans.,,, In 2008 Lenski's group reported that after more than 15 years and 30,000 generations of growth one of the E. coli cell lines suddenly developed the ability to consume citrate,,, the authors argued it might be pretty important.,,, They also remarked that,,, perhaps the mutation marked the beginning of the evolution of a brand new species.,, One scientist who thought the results were seriously overblown was Scott Minnich, professor of microbiology at the University of Idaho ,,, So Minnich's lab re-did the work under conditions he thought would be more effective. The bottom line is that they were able to repeatedly isolate the same mutants Lenski's lab did as easily as falling off a log -- within weeks, not decades.,,, Richard Lenski was not pleased.,,, In a disgraceful move, Lenski impugned Scott Minnich's character. Since he's a "fellow of the Discovery Institute" sympathetic with intelligent design,,, (Regardless of the ad hominem) With regard to citrate evolution, the Minnich lab's results have revealed E. coli to be a one-trick pony.,,, The take-home lesson is that,,, (Lenski's overinflated) hype surrounding the (implications of the citrate adaptation) has seriously misled the public and the scientific community. It's far past time that a pin was stuck in its (Lenski's citrate) balloon. http://www.evolutionnews.org/2016/05/richard_lenski102839.html
Of further note, besides the preceding failure for Darwinian theory on the molecular level of bacteria, I've always found wd400's selective extrapolation of what was happening in bacteria on the molecular level, to what was happening in on the molecular level of multicellular creatures, to be severely unwarranted. Especially since bacteria have never been shown to have the 'unlimited plasticity' that he presupposes them to have. An 'unlimited plasticity' for bacteria that he must first empirically demonstrate to be true for bacteria if he wants his extrapolation to multicellular creatures from bacteria to have any real scientific legitimacy:
Scant search for the Maker Excerpt: But where is the experimental evidence? None exists in the literature claiming that one species has been shown to evolve into another. Bacteria, the simplest form of independent life, are ideal for this kind of study, with generation times of 20 to 30 minutes, and populations achieved after 18 hours. But throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another, in spite of the fact that populations have been exposed to potent chemical and physical mutagens and that, uniquely, bacteria possess extrachromosomal, transmissible plasmids. Since there is no evidence for species changes between the simplest forms of unicellular life, it is not surprising that there is no evidence for evolution from prokaryotic to eukaryotic cells, let alone throughout the whole array of higher multicellular organisms. – Alan H. Linton – emeritus professor of bacteriology, University of Bristol. http://www.timeshighereducation.co.uk/story.asp?storycode=159282 The Paradox of the “Ancient” (250 Million Year Old) Bacterium Which Contains “Modern” Protein-Coding Genes: Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ; “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” http://mbe.oxfordjournals.org/cgi/content/full/19/9/1637 AMBER: THE LOOKING GLASS INTO THE PAST: Excerpt: These (fossilized bacteria) cells are actually very similar to present day cyanobacteria. This is not only true for an isolated case but many living genera of cyanobacteria can be linked to fossil cyanobacteria. The detail noted in the fossils of this group gives indication of extreme conservation of morphology, more extreme than in other organisms. http://bcb705.blogspot.com/2007/03/amber-looking-glass-into-past_23.html
The preceding certainly puts a damper on wd400s extrapolation from bacteria to multicellular creatures. Perhaps wd400 thinks he is above experimental reproach? I don't know. But what I do know is that wd400 takes the flimsiest of experimental support that might support evolution and makes grandiose claims for the unquestioned validity of evolution, all the while he completely ignores many other more substantial lines of evidence that refute his grandiose claims for evolution. Simply put, wd400 is exceptionally prone to what is known as 'confirmation bias'. Here is a supplemental note from Sanford:
The waiting time problem in a model hominin population - 2015 Sep 17 John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,, Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information. While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man. It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/
bornagain77_{October 26, 2016
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wd400: Wikipedia on the L-D experiment:
In their experiment, Luria and Delbrück inoculated a small number of bacteria (Escherichia coli) into separate culture tubes. After a period of growth, they plated equal volumes of these separate cultures onto agar containing the T1 phage (virus).
Here's what you wrote about this experiment:
For instance, if you tried to understand the LD experiment you would know the population starts from a single cell.
You don't know what you're talking about. Reread what I wrote. The argument still stands. The important point is that a study showed that in any bacterial population, the gene frequency of any allele never gets to 'zero'.PaV_{October 26, 2016
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Why do you do this? You just now:
We’re not arguing here about whether a clone produced a mutation or not—that is simply obvious ...
What you argued:
So, instead of “knowing” that a “mutation” occurs in the promoter region and, thus, adapting the bacterial population to a new environment, it might simply be that a ‘remnant’ of the bacterial form which is suited to the new environment simply begins to exponentially grow, while, at the same time, the original population begins to die away.
wd400_{October 25, 2016
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wd400: I just now ran across this putative answer of yours. Please let me respond: First,
If you really think mainstream evolutionary biology is like fascism then I encourage you to step back from this a little bit and get some perspective.
Look back at the post: I stated explicitly that you should look at the film, "Expelled." Ben Stein, an economist and comedian, and film actor, came across the turmoil at the Smithsonian, where a Confessional committee deemed that Sternberg's rights were violated, and ended up making a film. The film ends in Nazi Germany. "If the shoe fits, wear it."
As to the rest. I reads a lot like someone googling up pages and scanning them for passage they think support their view. For instance, if you tried to understand the LD experiment you would know the population starts from a single cell. All variation in the population is the result of mutation from that clone, it is not possible that a trait is carried over from a previous environment, it had to be generated by a new mutation. You then talk about directed mutation, apparently without undertstanding what happened to that line of research.
Subtlety is lost on you; even when it isn't so subtle. We're not arguing here about whether a clone produced a mutation or not---that is simply obvious--we're arguing about whether or not the mutation was 'random' or not. You've either missed the point, or chosen to miss the point.
So. Again. If you really think all these speculative theories hold any water, you would make a better argument for them if you demonstrated some understanding of the biology they attempt to explain.
You don't want me to "demonstrate some understanding of the biology," you want me to "understand" it the way you do. There's a word for this: orthodoxy, or, rather, dogma.PaV_{October 25, 2016
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If you really think mainstream evolutionary biology is like fascism then I encourage you to step back from this a little bit and get some perspective. As to the rest. I reads a lot like someone googling up pages and scanning them for passage they think support their view. For instance, if you tried to understand the LD experiment you would know the population starts from a single cell. All variation in the population is the result of mutation from that clone, it is not possible that a trait is carried over from a previous environment, it had to be generated by a new mutation. You then talk about directed mutation, apparently without undertstanding what happened to that line of research. So. Again. If you really think all these speculative theories hold any water, you would make a better argument for them if you demonstrated some understanding of the biology they attempt to explain.wd400_{January 11, 2016
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wd400:
Really? You are actually trying to compare mainstream evolutionary biology to Nazism?
No. I'm trying to compare it to "fascism." As you know, "fascists" censor the ideas of their opponents. Maybe you should watch the movie, Expelled. wd400:
That aside, citations (lizards diets and bacterial populations) hold rather more weight when you actually cite something more than your memory.
To test the effect of an “artificial” arthropod diet on gut morphology, we compared the digestive tracts of freshly caught, preserved Pod Mrc?aru lizards with those of preserved lizards of the same provenance that had been fed an exclusively arthropod diet for 15 wk. MANCOVA found no sex x diet interaction effect ( , ) and no difference be- [F1, 21 p 0.51 P p 0.79] tween the sexes ( , ), but the diet effect was [F6, 22 p 0.97 P p 0.47] highly significant ( , ). Results of univariate [F6, 23 p 7.55 P ! 0.001] ANCOVA can be found in Table 2. Lizards maintained on an arthropod diet showed a reduction in the weight of the small intestine and the hindgut. In addition, we found no evidence of cecal valves in any of the twenty specimens that had been fed arthropods. This was in sharp contrast to the high proportion (12/16) of individuals with valves among the freshly caught individuals (Pearson x2; , ) For more, here's the paper, Anatomical and Physiological Changes Associated with a Recent Dietary Shift in the Lizard Podarcis sicula, Bart Vervust, et. al.. From the same paper:
Our results suggest that in P. sicula, at least some of the changes associated with a dietary shift toward a higher proportion of plant material may be plastic. Specimens from the Pod Mrcaru population, which in nature eat substantial amounts of plant material (Herrel et al, 2008), exhibited a reduction in digestive tract length and a total loss of cecal valves after having been fed an exclusively arthropod diet for 15 wk. Although parts of their gastrointestinal systems were still better developed than those of specimens feeding mainly on arthropods in the wild, it seems likely that a prolonged exposure to an animal-based diet would have erased even those differences. These observations call for a more flexible view of the digestive system in lizards.
wd400:
Darwin’s Finches adapt form standing variation, so are not waiting for mutations.
Then NS is not based on "random mutations," right? There goes Darwinism. Oops! wd400:
You[r] bacterial example seems to forget the Luria–Delbrück experiment (of 1943) in which a single clone starts the population (an experiment that is repeated in ungergraduate labs to this day). The genome is replicated during asexual reproduction.
My reply to this distraction is the following: First, to frame what is going on here, and what is at stake: Barry Hall: 1988:-------------“Adaptive Evolution That Requires Multiple Spontaneous Mutations. I. Mutations Involving an Insertion Sequence”
As a result, we discuss mutation rates as though they were constants, generally related to cell division, that reflect only the properties that are inherent in the genome of the cell. We 896 B. G. Hall have ignored the possibility that mutation rates might be highly variable and subject, like other cellular processes, to environmental modulation. These results suggest that spontaneous mutation is a more complex process than we have believed, that mutation rates are not biological constants, and that probabilities of mutation are modulated by normally encountered environmental factors. The second lesson is that evolutionary biologists need to critically examine the assumptions that underlie methods of deducing evolutionary rates and of constructing phylogenetic trees. If the same mutation can, under appropriate selective conditions, occur in a large number of independent individuals (as occurs with excision of IS103 from within bglF), then individuals that share derived characters are not necessarily more closely related to each other than they are to other members of the population. If the probabilities of particular mutations are subject to environmental modulation, then the number of observed differences between two sequences may be completely unrelated to the time since they diverged.
All of this is completely consistent with my position. Further, the italicized portion points---already in 1988---to the problems evolutionary biologists would have in constructing “phylogenetic trees.” ................**********************************....................... Now, as to your specific point:........................................ Lenski, Slatkin, Ayala PNAS 1989 Mutation and selection in bacterial populations: Alternatives to the hypothesis of directed mutation From the Abstract:
Bacterial populations have served as model systems for studying evolutionary processes ever since the classic experiments of Luria and Delbruck, which demonstrated the occurrence of mutations prior to selection for the traits they conferred. However, several authors have recently presented experiments suggesting that bacteria may have mechanisms for directing which mutations occur, such that the rate of adaptive mutations is enhanced.
The bolded section makes it obvious that there is no discrepancy with what I claimed about small remnants of ‘variants,’ and this distribution. In fact, it SHOULD give rise to the “jackpot” distribution. This should have been clear to you almost immediately. Again, from “Lenski, Slatkin, and Ayala.”
The alternatives to the hypothesis of directed mutation that we have presented involve selection acting at the level of individuals within populations. By contrast, the processes hypothesized by Cairns et al. (3) and by Stahl (20) require selection acting on molecular variants within cells. There is an extensive literature in evolutionary biology concerning the potential for selection to act at different levels of organization (21-25). We do not reject outright the potential for selection acting on molecular variation within cells to produce changes in gene frequency. Rather, we argue that any plausible hypothesis to account for the types of observation reported by Cairns et al. (3), Hall (4), and Shapiro (5) must distinguish between the generation of variation and selection, at whatever levels of biological organization. Cairns et al. (ref. 3, p. 145) assert that directed mutation in bacteria (if it is demonstrated to exist) "could, in effect, provide a mechanism for the inheritance of acquired characteristics."
The names of these authors are so interesting---especially that of James Shapiro. So, there is the IN-GROUP: Lenski, and his lab. Ayala, and his textbook. And then the OUT-GROUP: Cairns, and Hall and Shapiro. But more than twenty years later, Shapiro writes a book about all of this called Evolution: a View from the 21st Century, in contrast, of course, to the late 19th, or early 20th century view. What great perspective this all provides. Thank you, wd400, for this great opportunity to learn what has really been going on behind the scenes for the last twenty-five years.
[Lenski, et. al. continue] The case against the inheritance of acquired characteristics was made by August Weismann (1834-1914), who observed that, in animals, the hereditary material is contained in the nucleus: "heredity is brought about by the transmission from one generation to another of a substance with a definite chemical . . . constitution" (27). Moreover, Weismann had noticed that the germ-line cells of animals are segregated early in the life of the individual, and he argued that there is no mechanism by which acquired modifications of the somatic cells could be transmitted to the nuclei of the germ cells.
Isn’t it interesting that this very issue has already come up in our discussion here. This simply underlines the power of the point I made to you above: Without the germline-soma split, the idea that ‘all’ of inheritance is to be found in the DNA of the germline would not have become entrenched, nor would it have led to Fisher and Wright’s view of things.. You seemed unable to make this rather obvious connection. Why? Lenski, et. al., continue:
Therefore, even if directed mutation were demonstrated in bacteria, this would not support in any manner whatsoever the traditional notions of Lamarck and his followers concerning the acquisition of adaptive characteristics. . . . ....................... Moreover, any confusion between the two may perpetuate mistaken beliefs concerning heredity that are still widely held outside scientific circles.
IOW, watch out for those ‘creationists’! As Dr. Cornelius Hunter often reminds us: “science is about religion. And religion really matters.” Finally, I happened to find an interesting blog by Jeffrey Dach, MD.
James A Shapiro Natural Genetic Engineering and Evolution, Part Two In part one we discussed how advances in science had rendered portions of Darwin’s Original 1859 theory antiquated and obsolete. In addition, a later revision of Darwin, neo-Darwinism updated with new knowledge of genetics, has also been rendered obsolete by new scientific understandings in molecular biology and cytogenetics.
What an interesting quote. It seems I’ve heard this very same thing written on this very post, right? Here’s some more:
Darwin acknowledged that sudden changes in evolution could occur independently of natural selection . He wrote: “… variations which seem to us in our ignorance to arise spontaneously. It appears that I formerly underrated the frequency and value of these latter forms of variation, as leading to permanent modifications of structure independently of natural selection“ (Origin of Species, 6th edition, Chapter XV, p. 395, emphasis added by Dr James A Shapiro). Dr Shapiro points out that the modern science of cytogenetics and molecular genetics has provided insight into biological novelties arising “independently of natural selection — hybridization, genome duplication, symbiogenesis, chromosome restructuring, horizontal DNA transfer, mobile genetic elements, epigenetic switches, and natural genetic engineering (the ability of all cells to cut, splice, copy, and modify their DNA in non-random ways). ” (2) “The genome sequence record tells us that these processes have accompanied rapid changes in all kinds of organisms. We know that many of them are activated by stress under extraordinary circumstances.”(2) Go look at the entire blogpost here. wd400:
We could go on like this. But, again, I really thing you should try and understand mainstream biology before you declare it’s not up to the task.
The critical word here is "mainstream." I suspect that James Shapiro is considered to be "out of the mainstream." You act as if all of this is settled, set in stone, when it's not. The evidence favors Shapiro, not Lenski; it's just a matter of time before things start changing.
PaV_{January 10, 2016
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The orthodoxy “must” prevail. “Heil Darwin!
Really? You are actually trying to compare mainstream evolutionary biology to Nazism? That aside, citations (lizards diets and bacterial populations) hold rather more weight when you actually cite something more than your memory. Darwin's Finches adapt form standing variation, so are not waiting for mutations. You bacertial example seems to forget the Luria–Delbrück experiment (of 1943) in which a single clone starts the population (an experiment that is repeated in ungergraduate labs to this day). The genome is replicated during asexual reproduction. We could go on like this. But, again, I really thing you should try and understand mainstream biology before you declare it's not up to the task.wd400_{January 9, 2016
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wd400:
Gene-environment interaction has been a major topic in evoluionary biology since the 1920s at least (that’s why quantative genetics, and as a result much of statistics, was invented).
This is a real head-scratcher. R.A. Fisher's goal was to take statistical mechanics and apply it to populations. Kimura used the "diffusion equation," which is a version of the Fokker-Planck equation. Provine talks about this in "Random Genetic Drift."
Gene regulation has been a major topic in molecular biology since at least the 1970s. There are many many examples of how genes can encode responses to environmental cues (indeed the paper I linked to at the start of this thread is one example of an environmental response requiring a particular allele).
And what is the logical progression at play here? Have you thought about that? First DNA is isolated as the source of proteins and life. Then, via Jacob-Monod and the lac operaon, a means of "controlling/regulating" the expression of genes is discovered. It involves a promoter region. Given neo-Darwinian thought, this was a logical progression. However, the jury, IMHO, is still out on this. Why? Because in a study a few years back, scientists investigated whether or not "gene frequencies" actually reached 100% in bacterial populations. Guess what? They found that it didn't. There were always tiny remnants of other forms of the bacterial population. So, instead of "knowing" that a "mutation" occurs in the promoter region and, thus, adapting the bacterial population to a new environment, it might simply be that a 'remnant' of the bacterial form which is suited to the new environment simply begins to exponentially grow, while, at the same time, the original population begins to die away. As I say: the jury is out. As always, you would rather declare victory than understand any of this, so you claim all the IDists need do is wait. Just a little longer. This time. ID is a way of guiding research; it is not, nor can it ever be (I don't think) a "theory." This in no way minimizes it's utility, however. Neo-Darwinism guides biology in the wrong direction. Not that progress isn't made, but that it is slowed down by the defective methodology it presents. Here is an example: [From Wikipedia on "Gene Regulation"]
Gene regulation is essential for viruses, prokaryotes and eukaryotes as it increases the versatility and adaptability of an organism by allowing the cell to express protein when needed. Although as early as 1951, Barbara McClintock showed interaction between two genetic loci, Activator (Ac) and Dissociator (Ds), in the color formation of maize seeds, the first discovery of a gene regulation system is widely considered to be the identification in 1961 of the lac operon, discovered by Jacques Monod, in which some enzymes involved in lactose metabolism are expressed by E. coli only in the presence of lactose and absence of glucose.
Notice two things: (1) Barbara McClintock was onto "gene regulation" first. (2) It didn't come into the mainstream of biology until at least a decade later (the 1970's per your description). Do you know why this discovery of McClintock had to wait? Because she wrote a paper describing "non-random" interactions within the chromosomes. And then what happened? Well, then J.B.S. Haldane, the leading light of population genetics at the time, publicly said that she 'obviously didn't understand the theory underlying genetics.' And what did McClintock do? She left the field of genetics. The orthodoxy "must" prevail. "Heil Darwin!" You can read about it in Provine's "Random Genetic Drift." [Her original paper can also be found online.] As far as "waiting," all the Darwinists had to do was "wait" for ENCODE to finish its study and confirm that the genome is mostly "junk." Oops! That didn't happen, did it? No. But can Darwinism ever be proven wrong? No. Of course not. Instead, the authors of ENCODE---just as in the case of Barbara McClintock---are publicly upbraided, and told they 'obviously don't understand what biological "function" is.'
For the lizards. I think I’ve told you multiple times that I don’t know how that trait arose, and we don’t have enough information to decide one way or another. The way to test it would be to measure standing variation in the source populations, and the heritability of the traits in question in both environments and across environment. After those sudies you could use genomic methods to dissect molecular basis of the changes.
This makes me want to tear my hair out. "Standing variation"? "Molecular basis of the changes"? This is simply your allegiance to the orthodoxy you're wedded to. The lab results are rather unmistakable. When you feed lizards a certain diet in the lab, and then, after a few WEEKS, they develop cecal valves, then you can be sure you're not dealing with Mendelian inheritance. Further, when you're dealing with a very small population of lizards who but weeks later make these tremendous phenotypic changes, you can be sure that a "mutation" is not involved. Again, for the umpteenth time, all of this points to what James Shapiro calls NGE. Population genetics becomes nothing but "white noise" compared to what's going on.
Those sorts of studies have been down on Darwin’s finches, so we know for sure those changes are not simply “environmental cues bringing this all about”.
A February 2015 study shows that the ALX1 gene is involved. Mutations of this transcription factor in humans has devastating effects. So, this is likely another confirmation of Behe's "First Principle of Adaptation." Nonetheless, a gene is clearly involved. Sequencing has established this. I remember reading about this paper when it came out. Nonetheless, how do we know where this mutation comes from? Beak sizes change in very short periods of time. When there are drought years, the finches don't reproduce. So, we're looking at, generously, 17 years, and with a population that is what---300? 500? probably less. So, 200 mutation per individual/generation. Then, for 20 years, and 500 finches, that's 2 x 5 x 2 x 10 x 10^2 x 10^2 = 2 x 10^6 Total mutations. And the genome size? I don't know, but I bet it's at least 10^9 nucleotides. Based on the numbers, we would 'likely' need a thousand times more breeding. So where did this "mutation" come from? Is it possible that there is a mechanism within the genome which, in response to environmental conditions, brings about mutations at a very high rate in certain parts of this specific gene? Yes, it's possible. (Let's remember that the Kimono Dragon can self-fertilize. How do get a "mutation" to do this when mutations come, supposedly, from the inaccurate replication of the genome; yet, the genome here wasn't replicated) But now we're talking about "natural genetic engineering," and not the Modern Synthesis. Again, the jury is out. And the answers the Darwin camp give simply don't look good, or convincing. Change is in the air. (But not until such time as the reins on the laboratories and classrooms around the world are loosened. What did Planck say about new 'paradigms'?)PaV_{January 9, 2016
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And now layers of regulatory mechanisms, triggered by environmental cues: how do you plan to explain all of this? Gene-environment interaction has been a major topic in evoluionary biology since the 1920s at least (that's why quantative genetics, and as a result much of statistics, was invented). Gene regulation has been a major topic in molecular biology since at least the 1970s. There are many many examples of how genes can encode responses to environmental cues (indeed the paper I linked to at the start of this thread is one example of an environmental response requiring a particular allele ). As always, you would rather declare victory than understand any of this, so you claim all the IDists need do is wait. Just a little longer. This time. For the lizards. I think I've told you multiple times that I don't know how that trait arose, and we don't have enough information to decide one way or another. The way to test it would be to measure standing variation in the source populations, and the heritability of the traits in question in both environments and across environment. After those sudies you could use genomic methods to dissect molecular basis of the changes. Those sorts of studies have been down on Darwin's finches, so we know for sure those changes are not simply "environmental cues bringing this all about".wd400_{January 9, 2016
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wd400:
Your support for the idea whole of evolutionary biology is about to collapse is a 5 year old paper that shows RNAs produced from a genome-encoded response can stick around (in round worms at least) for several generations.
First, just go back and reread the sections of the paper I included above. Not very good for your side. Then there's this about those lizards:
“As a result, individuals on Pod Mrcaru have heads that are longer, wider and taller than those on Pod Kopiste, which translates into a big increase in bite force,” says Irschick. “Because plants are tough and fibrous, high bite forces allow the lizards to crop smaller pieces from plants, which can help them break down the indigestible cell walls.”
And what is it that is supposed to prop-up pop. gen. and with it Darwinism: industrial melanism and the beak sizes of the Galapagos finches. What is documented to have happened in those lizards amounts to a greater phenotypic effect than in either the finches or Biston bistulleria. It is likely that there are environmental cues bringing this all about. And if this is confirmed, what then? Darwinism is a "house of cards." It's about to collapse. Someone just has to exhale strongly.PaV_{January 8, 2016
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wd400: It's the first paper that showed up on the radar. There are plenty of others. Just go look. As to "overwhelming," did you not notice the qualifier: "perhaps"? That you write RNAs produced from a genome-encoded response without a second thought, simply shows that you're fixated in your view of how the world of biology operates. Two things that ID would predict are: (1) that the vast majority of DNA would have function; and (2) that DNA that codes for genes is actually secondary to regulatory regions. We see this happening before our very eyes. It means nothing to you. The Darwinian view would say: (1) "junk" is to be expected, and (2) everything revolves around 'genes' and the regulation of 'genes.' While the second point in each might seem almost the same, they are actually very different. It is not a question of whether or not DNA is regulated---that is a given. It is a question of what is more fundamental to life itself. ID says it is "regulation"---something that is complex; Darwinism says it is the 'genes,' and "secondarily" the regulation of those genes. The ID view, articulated by myself and others for over 11 years here at UD, is the following analogy: in the construction of life's complexity, the 'genes' are a "tool set," while the regulatory mechanisms are the "blueprint." Darwin is a 'gene-centric' view. And experiments by the bundle show that there are "encoded" responses---not responses that are driven by neutral drift or random genetic drift, or mutation and selection; but, built-in responses. Here's an example: the Adriatic Lizard. I was wondering why everytime I brought this subject up, you stopped posting. Then I found an article where, by strict diet alone, lizards in the lab changed drastically---within weeks. If you care to, you will find that when the original article concerning the experiment on Pod Mrcaru and Pod Kopiste, I posted about it right here at UD. It was 2007, I believe. I suggested right there and then that this had to have been driven by an environmental cue. Even one of the regular UD commentors gave me a hard time. He asked whether I thought this was Lamarkian. I said that, no, it was epigentic. I went on to say that some enterprising experimenter ought to run an experiment where the food intake of the lizard was controlled. You want to call this "phenotypic plasticity," a vocabulary word that simply 'papers over' the cunundrum it represents. How utterly facile. But the problem remains: pop. gen. cannot explain how what happened did so so quickly. Since, the numbers didn't add up in this case. It was obvious that some internal mechanism was at play. Common sense would tell you that some internal, self-regulatory mechanism was at play. And it turned out to be exactly as I "predicted." The same common sense should tell any "objective" viewer that the foundations of pop. gen. is crumbling before our very eyes. Kimura couldn't explain so many polymorphisms in the genome. And now layers of regulatory mechanisms, triggered by environmental cues: how do you plan to explain all of this? Or will you simply try to sweep it under the rug for as long as you can? Maybe when the latest round of sequencing takes place they'll find "phlogiston." Darwinism is helpless to explain the rise of the complexity that everyday is discovered. Your situation is hopeless. It's only a matter of time.PaV_{January 8, 2016
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Your support for the idea whole of evolutionary biology is about to collapse is a 5 year old paper that shows RNAs produced from a genome-encoded response can stick around (in round worms at least) for several generations. From this small effect you get to "overwhelming" phenotypic change? When the authors themselves says it is 'conceivable' to 'speculate' that other examples might exist. Are you serious about this? Or have you just typed yourself into a position that you feel you have to defend?wd400_{January 8, 2016
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wd400:
You know the RNAs come from DNA, right?
What do you mean. OOL people tell us that RNA came first. So, it's DNA from RNA. More seriously, look at the article I linked to above in answer to Jonas. It's from 2011. "Extrachromosomal" inheritance; maybe 'common'; controlling other functions! IOW, phenotype is affected---perhaps in an overwhelming way---in "non-Mendelian" ways. Where does that leave pop. gen. exactly?PaV_{January 8, 2016
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Jonas: Here's the lowdown: You can access this Cell article from 2011: Transgenerational Inheritance of an Acquired Small RNA-Based Antiviral Response in C. elegans by Oded Rechavi, Gregory Minevich, and Oliver Hober
We have described here a series of genetic experiments that provide support for the existence of non-Mendelian, multigenerational inheritance of extrachromosomal information. This information is transmitted in the form of small RNAs, viRNAs, which are induced by an episode of viral replication and which are propagated through the germline in a non-template-dependent manner. Our results therefore support the Lamarckian concept of the inheritance of an acquired trait. . . . It is conceivable that other biological functions may be controlled by transgenerationally transmitted, extrachromosomal agents as well. For example, one may speculate that the recently described inheritance of an olfactory memory (Remy, 2010) or the transgenerational inheritance of longevity traits (Greer et al., 2011) could also be the result of inherited small RNA molecules. Intriguingly, our deep sequencing of rde-4( / ) animals not only identified transgenerationally transmitted viRNA molecules but also suggests that several classes of rde-4-dependent endo-siRNAs may be inherited (O.R., G.M., and O.H., unpublished data), indicating that the transmission of extrachromosomal information may be a common phenomenon.Such a mode of inheritance may provide adaptive advantages to an animal.
You will notice that this is "non-Mendelian," passed along for generations, possibly common, possibly controlling other "functions" in an "extrachromosomal" manner, and tied to "fitness." What more could one possibly do to undermine Fisher's hypothetical model?PaV_{January 8, 2016
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Jonas- Nick Lane's "The Vital Question" pretty much dispenses with the "genes/ environment" stance. I just started it though...Virgil Cain_{January 7, 2016
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PaV, thank you for your responses.Maybe I am dense (a distinct possibility) but I still don't see how environmentally mitigated expression of genes will not be significantly impacted by a change in allele frequency. Maybe an overly simplified example might make my point clearer. Or make it clearer that I am not understanding the issue. Let's assume that gene A results in phenotype A! under one environmental trigger 1 and phenotype A^ under environmental trigger 2. If a mutation in gene A results in improved fitness for phenotype A! and no change in fitness for phenotype A^, then the mutation is more likely to become fixed if the population is predominantly exposed to trigger 1 than it would if it was predominantly exposed to trigger 2. This, as far as I know still follows what we know about natural selection and population genetics. Am I getting this all wrong?Jonas Crump_{January 7, 2016
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It’s that simple. RNA mediated changes in phenotype, is not DNA mediated changes in phenotype. You know the RNAs come from DNA, right?wd400_{January 7, 2016
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Jonas: But it is still the genes being expressed that result in the phenotype. As such, wouldn’t a change in allele frequencies result in a change in phenotype? If I may but in: I've already mentioned that without proteins, life isn't going to happen. And without DNA, which specifically codes for the proteins, life is not going to happen. But we're dealing here not with the question: where do proteins come from? nor even, does the environment affect DNA expression? These are all 'givens.' The question is this: what mechanism is involved through which the environment and DNA interact. The Darwinian solution is that "mutations" occur. [One could generalize this and called them "variations", including recombination, so-called 'gene duplication', and, of course, SNPs (single nucleotide polymorphisms)] These "mutations", then, cause a changed protein, or a changed expression, or both, and this causes an increase in fitness. If this were all there was, then you could allege that through 'trial and error,' Darwinian evolution will proceed, and newer forms develop. However, here, this linkage between DNA and 'fitness' (i.e., the environment) is broken. Now we don't have "mutations" leading to phenotypic change, but other mechanisms. With that, the Darwinian scaffolding collapses. Population genetics collapses, too, intertwined as they are. It's that simple. RNA mediated changes in phenotype, is not DNA mediated changes in phenotype. And with that, neo-Darwinism loses much of its impact, which, according to Behe's "The Edge of Evolution," wasn't much to begin with.PaV_{January 7, 2016
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VC, isn't that an example of what I was saying? The final form is the result of an interaction of the DNA (genes) and the environment. I assume that the iodine triggers or suppresses or delays the expression of one gene or more, resulting in a different phenotype. But it is still the genes being expressed that result in the phenotype. As such, wouldn't a change in allele frequencies result in a change in phenotype?Jonas Crump_{January 7, 2016
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As for epigenetics, there exists a salamander in Mexico- the Axolotl. Itb was a local delicacy- believe it or not. Someone took samples back to France so that the French could enjoy them too. However the pond they were put in was rich in iodine and guess what? The Axolotl is an immature form of the salamander and yet it can reproduce as if it is another species (neoteny)! The iodine in the pond triggered further development into its adult form. People thought they were two different species!!Virgil Cain_{January 7, 2016
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It isn't just me, Jonas: Chapter VI “Why is a Fly not a horse?” (same as the book’s title)
”The scientist enjoys a privilege denied the theologian. To any question, even one central to his theories, he may reply “I’m sorry but I do not know.” This is the only honest answer to the question posed by the title of this chapter. We are fully aware of what makes a flower red rather than white, what it is that prevents a dwarf from growing taller, or what goes wrong in a paraplegic or a thalassemic. But the mystery of species eludes us, and we have made no progress beyond what we already have long known, namely, that a kitty is born because its mother was a she-cat that mated with a tom, and that a fly emerges as a fly larva from a fly egg.”- geneticist Giuseppe Sermonti
And
To understand the challenge to the “superwatch” model by the erosion of the gene-centric view of nature, it is necessary to recall August Weismann’s seminal insight more than a century ago regarding the need for genetic determinants to specify organic form. As Weismann saw so clearly, in order to account for the unerring transmission through time with precise reduplication, for each generation of “complex contingent assemblages of matter” (superwatches), it is necessary to propose the existence of stable abstract genetic blueprints or programs in the genes- he called them “determinants”- sequestered safely in the germ plasm, away from the ever varying and destabilizing influences of the extra-genetic environment. Such carefully isolated determinants would theoretically be capable of reliably transmitting contingent order through time and specifying it reliably each generation. Thus, the modern “gene-centric” view of life was born, and with it the heroic twentieth century effort to identify Weismann’s determinants, supposed to be capable of reliably specifying in precise detail all the contingent order of the phenotype. Weismann was correct in this: the contingent view of form and indeed the entire mechanistic conception of life- the superwatch model- is critically dependent on showing that all or at least the vast majority of organic form is specified in precise detail in the genes. Yet by the late 1980s it was becoming obvious to most genetic researchers, including myself, since my own main research interest in the ‘80s and ‘90s was human genetics, that the heroic effort to find information specifying life’s order in the genes had failed. There was no longer the slightest justification for believing there exists anything in the genome remotely resembling a program capable of specifying in detail all the complex order of the phenotype. The emerging picture made it increasingly difficult to see genes as Weismann’s “unambiguous bearers of information” or view them as the sole source of the durability and stability of organic form. It is true that genes influence every aspect of development, but influencing something is not the same as determining it. Only a small fraction of all known genes, such as the developmental fate switching genes, can be imputed to have any sort of directing or controlling influence on form generation. From being “isolated directors” of a one-way game of life, genes are now considered to be interactive players in a dynamic two-way dance of almost unfathomable complexity, as described by Keller in The Century of The Gene- Michael Denton “An Anti-Darwinian Intellectual Journey”, Uncommon Dissent (2004), pages 171-2
Yes, it looks like there is something else that determines the phenotype. If ID is correct that something else would be softwareVirgil Cain_{January 7, 2016
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Jonas: I am simply a fairly informed layman in this field. I am no expert, and cannot give you an expert opinion. Certainly, years ago, once the 'code' was broken, they had to have very quickly understood that the DNA of one cell is the same as that for another. How do you explain it? Expression and non-expression, which then gives rise to Monod's work with operons, where a 'gene' is switched 'on-and-off' to adapt bacteria to a particular environment. All of this would have fallen under the umbrella of "epigenetics." But there was a lot of other work, too, that fell into this view. (the effect of 'heat' on development was seen, and so we hear of 'heat shock' proteins now; soil conditions also affected development) But, basically, it was one 'gene' regulating another 'gene'---the'sensitivity' of the controlling 'gene,' which would interact with the environment directly, could be turned 'on-and-off.' Then the idea of 'gene networks' arose since it was seen that in particular cases more than one 'gene' is needed to give rise to expression. What's so different now is this: (1) it is now known that changes in an organism---changes in expression---can be transmitted from one generation to the next; and, not only that, but for a great many generations after; and (2) there is a whole slew of molecular machines---RNA directly interacting with DNA and other proteins---that can bring about differences in expression. These RNA, being RNAs, are obviously transmitted in a much different way than DNA. That's it in a 'nutshell.' Got to run.PaV_{January 7, 2016
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VC: "We don’t know what produces the phenotype. DNA/ genes influence development but do not determine what is developing." Are you suggesting that it is something other than the genes mitigated by environment?Jonas Crump_{January 7, 2016
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