Now that’s different: Identical twins, one in space, have different DNA?

Thanks TWSYF, but I should always preface statements like that with,,, "in the minds of Darwinists" Darwinism is a religion, not a testable science. Since, whether they accept it or not, Darwinism has been, none-the-less, falsified by experimentation and mathematics. For instance:

Michael Behe - Observed (1 in 10^20) Edge of Evolution - video - Lecture delivered in April 2015 at Colorado School of Mines 25:56 minute quote - "This is not an argument anymore that Darwinism cannot make complex functional systems; it is an observation that it does not." https://www.youtube.com/watch?v=9svV8wNUqvA

i.e. Although Darwinian evolution is constantly contradicted by observational evidences like this, "in the minds of Darwinists" that evidence is never allowed to falsify the theory.,,, hence, "in the minds of Darwinists" Darwinism is a religion, not a testable science. bornagain77

BA77 @ 43: "Darwinism is a religion, not a testable science." Well said. Truth Will Set You Free

as to:

It seems to me that these (Horizontal Gene Transfer and epigenetics) only strengthen Darwin’s theory.

News flash AK, Horizontal Gene Transfer and epigenetics, like the rest of the astonishingly intricate and elaborate processes being found in molecular biology, are certainly not friends of Darwinian evolution, i.e. of accidentally kludging things together.

Three Ways that Transposable Elements Demolish Evolutionary Theory - Cornelius Hunter - March 14, 2017 Excerpt: Transposable elements just don’t make sense. These so-called “jumping genes” are segments of junk DNA that insert themselves at random in our genomes. That is the evolutionary interpretation of these genetic units, but how and why do they move about, and why don’t they wreak havoc on the genome? The answers to these questions, which have been emerging in recent years, is that transposable elements are exquisite, finely tuned, highly functional molecular machines that contradict evolutionary expectations. Evolutionists have a long, failed history of presumed disutility — after all, the world arose by chance, surely it doesn’t work very well — and transposable elements are just one more example of this failed prediction. But the junk-to-hero story is only one of three ways that transposable elements utterly demolish evolutionary theory. The other two prongs in this Darwin-destroying triad are serendipity and pattern. By serendipity, I am referring to the rather awkward findings, which are undeniable at this point, that if evolution is true, then it must have come about by highly complex, non-adaptive, mechanisms. From diploid genetics to horizontal gene transfer, alternate gene splicing, genetic regulation, epigenetics, mechanisms that cause adaptive mutations, and transposable elements, evolution must have bumbled along by luckily constructing fantastically complex mechanisms. Those mechanisms would provide no immediate adaptive value, yet somehow would persist and become vital agents in evolutionary history. Simply put, evolution must have created evolution in a most unlikely (astronomically unlikely) set of circumstances. That’s serendipity, not science, and transposable elements heap more fuel onto the fire. By pattern, I am referring to another set of awkward findings, again undeniable, that the pattern of structures observed across the species consistently contradicts evolution’s predictions. One of those contradictions are the enormous differences found in otherwise allied species. All three of these contradictions — disutility, serendipity, and pattern — are on display in a new, systematic study of transposable elements out of Didier Trono’s lab in Switzerland. https://evolutionnews.org/2017/03/three-ways-that-transposable-elements-demolish-evolutionary-theory/ A Key Evidence for Evolution Involving Mobile Genetic Elements Continues to Crumble - Cornelius Hunter - July 13, 2014 Excerpt: A study published last week found strong signs of function in mobile repetitive DNA elements. Mobile genetic elements have been heavily recruited by evolutionists in recent years as powerful, undeniable proofs of common ancestry. An underlying assumption in those proofs, aside from the usual non scientific metaphysics, is that such mobile elements insert themselves into the genome at random.,,, The biological roles of these place-jumping, repetitive elements are mysterious. They are largely viewed (by Darwinists) as “genomic parasites,” but in this study, researchers found the mobile DNA can provide genetic novelties recruited as certain population-unique, functional enrichments that are nonrandom and purposeful. “The first shocker was the sheer volume of genetic variation due to the dynamics of mobile elements, including coding and regulatory genomic regions, and the second was amount of population-specific insertions of transposable DNA elements,” Michalak said. “Roughly 50 percent of the insertions were population unique.” http://darwins-god.blogspot.com/2014/07/a-key-evidence-for-evolution-involving.html DNA is life's blueprint? No, master controller of the cell - 13 June 2015 by Claire Ainsworth Everything we thought we knew about the genome is turning out to be wrong as The Deeper Genome and The Developing Genome make clear. New metaphors, anyone? Excerpt: Take DNA. It's no simple linear code, but an intricately wound, 3D structure that coils and uncoils as its genes are read and spliced in myriad ways. Forget genes as discrete, protein-coding "beads on a string": only a tiny fraction of the genome codes for proteins, and anyway, no one knows exactly what a gene is any more. A key driver of this new view is ENCODE, the Encyclopedia of DNA Elements, which is an ambitious international project to identify the functional parts of the human genome. In 2012, it revealed not only that the protein-coding elements of DNA can overlap, but that the 98 per cent of the genome that used to be labelled inactive "junk" is nothing of the sort. Some of it regulates gene activity, some churns out an array of different kinds of RNA molecules (RNAs for short), some tiny, some large, many of whose functions are hotly debated. Parrington quotes ENCODE scientist Ewan Birney as saying at the time, "It's a jungle in there. It's full of things doing stuff." And that is one of the most apt genome metaphors I've ever read. Recent insights into what some of this "stuff" is reveal problems with another classic idea: that DNA is the master controller of the cell, with information flowing in one direction from it, via RNA, to proteins. Some of ENCODE's mystery RNAs control gene activity, others make changes that the cell remembers and passes on when it divides, and which can even be passed down generations. The RNAs may be one way the environment alters the behaviour of genes without changing their DNA sequences, a phenomenon known as epigenetics. Growing evidence of the extent of epigenetic influence on the genome has led some researchers to argue that much of medical research, and indeed mainstream evolutionary theory, places too much importance on genes in determining an organism's characteristics. They think the environment plays a much bigger role in their emergence as an organism develops. ,,, But just as genes are not destiny, neither is epigenetics. Like Parrington, Moore warns against oversimplification. Epigenetic determinism is just as unhelpful as the deterministic gene-as-blueprint idea. "Do not assume you are trapped by your biology," he says. That genetics is complicated isn't news, but Parrington and Moore underline the limitations and the power of trying to understand its complexity by reducing it to simpler divisions. For example, the molecular and computing technologies spawned by such attempts are now giving researchers the potential to work out how to integrate it all to form a greater whole. Time, surely, to rip up the old metaphors and create some new ones. This article appeared in print under the headline "It's so last century!" http://www.newscientist.com/article/mg22630251.000-dna-is-lifes-blueprint-no-master-controller-of-the-cell.html#.VXySfUbcBCB How life changes itself: the Read-Write (RW) genome. - 2013 Excerpt: Research dating back to the 1930s has shown that genetic change is the result of cell-mediated processes, not simply accidents or damage to the DNA. This cell-active view of genome change applies to all scales of DNA sequence variation, from point mutations to large-scale genome rearrangements and whole genome duplications (WGDs). This conceptual change to active cell inscriptions controlling RW genome functions has profound implications for all areas of the life sciences. http://www.ncbi.nlm.nih.gov/pubmed/23876611 Revisiting the Central Dogma in the 21st Century - James A. Shapiro - 2009 Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112). http://shapiro.bsd.uchicago.edu/Shapiro2009.AnnNYAcadSciMS.RevisitingCentral%20Dogma.pdf

Also of interest from the preceding paper, on page 22, is a simplified list of the ‘epigenetic’ information flow in the cell that directly contradicts what was expected from the central dogma (Genetic Reductionism/modern synthesis model) of neo-Darwinism.

"It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works. All careful studies of mutagenesis find statistically significant non-random patterns” James Shapiro - Evolution: A View From The 21st Century - (Page 82)

In other words, Alan Keith's failure to see Horizontal Gene Transfer and epigenetics as a insurmountable problem for Darwinian theory, and indeed for him to claim that they "only strengthen Darwin’s theory" is yet more evidence of the pseudo-scientific nature of Darwinian theory in that no finding, at least in the minds of Darwinists, is ever allowed to falsify Darwinian theory. i.e. Darwinism is a religion, not a testable science. bornagain77

AK @ 40: HGT and epigenetic mechanisms aren't sources of variations, they're means of storing, communicating, and expressing variations. Moreover, they potentially remove the need for immediate variation generation, making RM+NS (and other errors held separately to confuse the issue) completely unnecessary to observed variation; beyond the coincidentally fortunate breaking of things. Likewise, they are themselves sophisticated functions that ultimately must be accounted for by RM+NS while operating several degrees beyond immediate selection, which is all that NS can pick from; they are far more of a challenge for mindless evolution than the features they accommodate. Not only that, but they require more tuning from the features that they accommodate, as those features must be sufficiently modular/communicable/formatted to work with them. Darwin was proposing what is essentially in the crudest class of genetic algorithm, and forcing it to work against a large and variable set of axes to produce results that it would be ludicrous to expect for far better genetic algorithms that are properly constrained to ever yield. The field of evolutionary simulation being strewn with the wreckage of cheats and lies is sufficient testament to this. Of course, without being able to even lay claim to observed variation, and without possessing any demonstrable, even simulable forward model, Darwin's theory isn't much of a theory. A hypothesis it remains, at best. LocalMinimum

Allan Keith: Yet HGT has been known about for over half a century, and the fact that gene expression is affected by environment has been known even longer.

You say this, as if problems are automatically solved when they are known for a long time. Unfortunately, that’s not the case. Back in 1904, Hugo de Vries wrote:

Natural selection is a sieve. It creates nothing, as is so often assumed; it only sifts. It retains only what variability puts into the sieve. Whence the material comes that is put into it, should be kept separate from the theory of its selection. How the struggle for existence sifts is one question; how that which is sifted arose is another.

“It creates nothing, as is so often assumed …”, wrote De Vries, and he is right, even of today’s conception. Still many Darwinians hold that the going out of existence of X, explains the existence of Y. However elimination (a.k.a. “natural selection”) explains only why some things are not, not why some things are. If natural selection is a process of elimination, then existent organisms are the ones that got away. Instead of being created by ‘natural elimination’, exactly the opposite is true: they are “untouched” by ‘natural elimination’. Existent organisms are those organisms on which natural selection has precisely no bearing whatsoever. They are the undiluted products of chance. Moreover, natural selection slows evolution down. Natural selection (NS) culls variety — eliminates organisms with certain traits from the population. In effect, NS enhances chances for the remaining variation. IOWs it intensifies a particular search and thereby enhances the probability of its success. Assuming that functional islands are not necessarily connected, the overall chance of finding evolutionary novelty remains the same, with or without NS, — the intensified search compensates for the loss of variety. However, the waiting time for the selected variation to restore the original population size is slowing down evolution. If some disease kills off all human race, except for the Japanese, then the probability of finding evolutionary novelties is restored at the moment that the Japanese have a population size of 7 billion. My point? The waiting time needs to be factored in. Origenes

LocalM,

As HGT and epigenetics explain more and more of the mechanics of life’s variety with precision that Darwin couldn’t conceive of, Darwin will be occupying smaller and smaller gaps.

It seems to me that these only strengthen Darwin’s theory. Remember that his theory is remarkably simple. Natural selection acting on the variability in s population to result in differential survival of traits. This required a source of this variability, which he knew nothing about, and the heritability of these traits, which again he knew nothing about. If either of these were found not to occur, his theory would be falsified. We know that “random” mutations are s source of variation. We later discovered other sources of variation, things like inversions, translocations, meiosis, HGT (including viruses), epegenetics, and others. All strengthen his theory. And with the discovery of DNA, we now know the means of inheritance. I fail to see how any of these discoveries weaken his theory. Allan Keith

AK @ 37: As HGT and epigenetics explain more and more of the mechanics of life's variety with precision that Darwin couldn't conceive of, Darwin will be occupying smaller and smaller gaps. LocalMinimum

Whatever AK, I've laid my case out in post 2 and 36 for why Darwinian theory is more properly classified as a pseudoscience rather than a real science, and will let readers decide for themselves who is being 'scientific' and who is blowing smoke. bornagain77

BA77,

Darwin’s pseudo-theory is forever plastic and is able to explain completely contradictory results with equal ease.

If you think that the flexibility of a theory is the sign of a weak theory then you don’t understand how science works. ID proponents throw out things like HGT and epigenesis as if they are newly discovered showstoppers. Yet HGT has been known about for over half a century, and the fact that gene expression is affected by environment has been known even longer. Neither of these are incompatible with natural selection acting on variation. Allan Keith

AK:

"don’t mistake unfalsifiable with modifiable."

HA HA HA :) Too funny. The only thing that anyone ever witnesses truly 'evolving' in the real world is the theory of Darwinian evolution itself. Darwin's pseudo-theory is forever plastic and is able to explain completely contradictory results with equal ease.

"Being an evolutionist means there is no bad news. If new species appear abruptly in the fossil record, that just means evolution operates in spurts. If species then persist for eons with little modification, that just means evolution takes long breaks. If clever mechanisms are discovered in biology, that just means evolution is smarter than we imagined. If strikingly similar designs are found in distant species, that just means evolution repeats itself. If significant differences are found in allied species, that just means evolution sometimes introduces new designs rapidly. If no likely mechanism can be found for the large-scale change evolution requires, that just means evolution is mysterious. If adaptation responds to environmental signals, that just means evolution has more foresight than was thought. If major predictions of evolution are found to be false, that just means evolution is more complex than we thought." ~ Cornelius Hunter

As William James Murray quipped, "Who would have thought that it would be biologists that came up with the first Theory of Everything?"

Who would have thought that it would be biologists that came up with the first Theory of Everything? Biological divergence? Evolution. Biological convergence? Evolution. Gradual variation? Evolution. Sudden variation? Evolution. Stasis? Evolution. Junk DNA? Evolution. No Junk DNA? Evolution. Tree of life? Evolution. No tree of life? Evolution. Common genes? Evolution. Orfan genes? Evolution. Cell with little more than a jelly-like protoplasm? Evolution. Cell filled with countless, highly-specified nano-machines directed by a software code? Evolution. More hardy, more procreative organisms? Evolution. Less hardy, less procreative organisms? Evolution. - Evolution explains everything. - William J Murray

Imre Lakatos, although he tipped toed around the failure of Darwinism to have a rigid demarcation criteria in science,,,

In his 1973 LSE Scientific Method Lecture 1[12] he (Lakatos) also claimed that “nobody to date has yet found a demarcation criterion according to which Darwin can be described as scientific”. http://en.wikipedia.org/wiki/Imre_Lakatos#Darwin.27s_theory A Philosophical Question...Does Evolution have a Hard Core? Some Concluding Food for Thought In my research on the demarcation problem, I have noticed philosophers of science attempting to balance (usually unconsciously) a consistent demarcation criteria against the disruptive effects that its application might have with regard to the academic status quo (and evolution in particular)… Few philosophers of science will even touch such matters, but (perhaps unintentionally) Imre Lakatos does offer us a peek at how one might go about balancing these schizophrenic demands (in Motterlini1999: 24) “Let us call the first school militant positivism; you will understand why later on. The problem of this school was to find certain demarcation criteria similar to those I have outlined, but these also had to satisfy certain boundary conditions, as a mathematician would say. I am referring to a definite set of people to which most scientists as well as Popper and Carnap would belong. These people think that there are goodies and baddies among scientific theories, and once you have defined a demarcation criterion. you should divide all your theories between the two groups. You would end up. for example, with a goodies list including Copernicus’s (Theory1), Galileo’s (T2), Kepler’s (T3), Newton’s (T4) … and Einstein’s (T5), along with (but this is just my supposition) Darwin’s (T6). Let me just anticipate that nobody to date has yet found a demarcation criterion according to which Darwin can be described as scientific, but this is exactly what we are looking for.” So basically, the demarcation problem is a fun game philosophers enjoy playing, but when they realize the implications regarding the theory of evolution, they quickly back off… http://www.samizdat.qc.ca/cosmos/philo/hardcore_pg.htm

,,, although Lakatos tipped toed around the failure of Darwinism to have a rigid demarcation criteria in science, Lakatos was brave enough to state that a good scientific theory will make successful predictions in science whereas “In degenerating programmes, however, (epicycle) theories are fabricated only in order to accommodate known facts”

Science and Pseudoscience (transcript) - “In degenerating programmes, however, theories are fabricated only in order to accommodate known facts” – Imre Lakatos (November 9, 1922 – February 2, 1974) a philosopher of mathematics and science, , quote as stated in 1973 LSE Scientific Method Lecture http://www2.lse.ac.uk/philosophy/about/lakatos/scienceandpseudosciencetranscript.aspx Here’s That Algae Study That Decouples Phylogeny and Competition - June 17, 2014 Excerpt: "With each new absurdity another new complicated just-so story is woven into evolutionary theory. As Lakatos explained, some theories simply are not falsifiable. But as a result they sacrifice realism and parsimony." - Cornelius Hunter http://darwins-god.blogspot.com/2014/06/heres-that-algae-study-that-decouples.html Darwin's (Failed) Predictions: An Interview with Cornelius Hunter, Part I and II http://www.evolutionnews.org/2009/06/darwins_failed_predictions_an021311.html http://www.evolutionnews.org/2009/06/darwins_failed_predictions_an_1021321.html

Thus the fact that the theory of Darwinian evolution is, in your words, 'modifiable', is actually, contrary to what you believe true for a scientific theory, more solid evidence that we are in fact dealing with a pseudoscience rather than a real science. bornagain77

BA77, don’t mistake unfalsifiable with modifiable. Since Darwin’s day his theory has been expanded on as new evidence and mechanisms were discovered. The fact that natural selection acting on variation still remains fundamental to the theory is a testament to the rigour of his original theory. Allan Keith

Well Allen Keith, seeing as Darwinian evolution is, at least how Darwinists treat it, a unfalsifiable pseudoscience,,,

As mentioned in post 2 https://uncommondescent.com/intelligent-design/now-thats-different-identical-twins-one-in-space-have-different-dna/#comment-653586

,,,then there is basically no experimental finding that will ever be 'paradigm shifting' for Darwinists. Darwinian evolution, since its inception, has been basically impervious to experimental falsification (again, at least how Darwinists treat their theory). bornagain77

This may be interesting research but it isn't exactly earth shattering, paradigm shifting news. https://www.scientificamerican.com/article/identical-twins-exhibit-d/ https://www.scientificamerican.com/article/identical-twins-genes-are-not-identical/ https://arstechnica.com/science/2014/12/finding-gene-activity-differences-in-identical-twins/ https://www.psychologytoday.com/blog/the-superhuman-mind/201211/identical-twins-are-not-genetically-identical https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063335/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC436052/ And that was only the first few of a Google search for "do identical twins have different gene expressions" that had 794,000 hits. Allan Keith

Some say this is a non-story: https://arstechnica.com/science/2018/03/scott-kellys-medical-monitoring-has-spawned-some-horrific-press-coverage/ Nonlin.org

I guess you are going to have to try and express yourself more clearly Origenes. Can you clearly state what you think is the challenge to mainstream biology in this? At the moment you have said "homeostasis" a lot, but not made an argument at all. cornu

cornu@

There are only a few hundred genes with apparently continued differential expression.

"Only" a few hundred, you say. And during space flight "only" a few thousand, I suppose.

Gene expression can be quite sloppy, so minor changes in transcript abundance may have little physiological effect.

"Quite sloppy", you say. Details do not matter much?

It’s a bit weird to ask how homeostasis can handle changes in gene expression. It’s quite possible that the changes in gene expression are homeostasis. Physiological cues brought about by strange food, lack of weight-bearing exercise etc giving rise to changes in gene expression.

Hmm ... to me it seems quite likely that Scott was familiar with 'space food' before he took off. "Lack of weight-bearing exercise etc", you say. Did you come up with that as an 'earthly equivalent' for the effects of weightlessness? :)

Hard to see the challenge to evolutionary biology there.

Well, let's wait and see if your "lack of weight-bearing exercise" can bring about a similar homeostatic (?) response.

I agree with others the telomere result is the most interesting. But I can’t see why this result is qualitatively different than the gene expression one. To lengthen telomeres, you just need to express more telomerase (as happens in cancer cells on earth).

Ah. So, harmless and no problem for homeostasis. Origenes

How was this n=1 in both arms study controlled? In my opinion it is just bugger all. Peer

Why is everyone fixated on DNA? DNA is not essence of life: http://nonlin.org/dna-not-essence-of-life/ Nonlin.org

So CR, do you really, really, really, believe that "knowledge laden genes" run the whole show in biology??? Perhaps it would help you to realize just how 'puppet-like' genes actually are in an organism. i.e. Despite the 'selfish gene' metaphor of Dawkins, genes are now known to not even be masters of their own fate much less the masters of everything else in biological organisms.

"Hundreds or thousands of DNA sequences move (or are moved) within vast numbers of cell nuclei, and are subjected to extraordinarily nuanced, locally modulated chemical activity so as to contribute appropriately to bodily requirements that are nowhere codified — least of all in those DNA sequences.,,," - Talbott

Or perhaps a larger dose of medicine is necessary for you CR:

Genes and Organisms: Improvising the Dance of Life - Stephen L. Talbott - Nov. 10, 2015 Excerpt: The performances of countless cells in your body are redirected and coordinated as part of a global narrative for which no localized controller exists. This redirection and coordination includes a unique choreography of gene expression in each individual cell. Hundreds or thousands of DNA sequences move (or are moved) within vast numbers of cell nuclei, and are subjected to extraordinarily nuanced, locally modulated chemical activity so as to contribute appropriately to bodily requirements that are nowhere codified — least of all in those DNA sequences.,,, DNA in its larger matrix You may recall from my earlier article, “Getting Over the Code Delusion” (Talbott 2010), that packing DNA into a typical cell nucleus is like packing about 24 miles of very thin, double-stranded string into a tennis ball, with the string cut up (in the normal human case) into 46 pieces, corresponding to our 46 chromosomes. To locate a protein-coding gene of typical size within all that DNA is like homing in on a one-half-inch stretch within those 24 miles. Or, rather, two relevant half-inch stretches located on different pieces of string, since we typically have two copies of any given gene. Except that sometimes one copy differs from the other and one version is not supposed to be expressed, or one version needs to be expressed more than the other, or the product of one needs to be modified relative to the other. So part of the job may be to distinguish one of those half-inch stretches from the other. “Decisions” everywhere, it seems. But no such decisions are made in a vacuum. As it happens, the chromosome does not consist of a naked DNA double helix. Our DNA, rather, is bound up with a massive, intricate, and dynamic protein-RNA-small molecule complex (called chromatin) that is as fully “informative” for the cell as the DNA sequence itself — and, you might say, much more active and directive.,,, the cell, by managing the shifting patterns of the chromatin infrastructure within which DNA is embedded, brings our chromosomes into movement on widely varying scales. These include large looping movements that put particular genes into connection with essential regulatory sequences and with other, related genes (that is, with other one-half inch stretches of our “24 miles of string in a tennis ball”).,,, A gene is not in any case the kind of rigidly defined entity one might hope to calculate with. As a functional unit appropriate to current circumstances, it must be cobbled together by the cell according to the needs of the moment. There is no neatly predefined path to follow once the cell has located the “right” half inch or so of string, or once it has done whatever is necessary to bring that locus into proper relation with other chromosomal loci participating in the same “dance”. One issue has to do with the fact that there are two strands in the DNA double helix and, starting from any particular point, it is possible to transcibe either of two DNA sequences in either of two directions: “forward” along one strand, or “backward” along the other. This yields two completely different products. One of them is very likely not even a protein-coding RNA, and yet it may still play a vital role in gene expression and in cellular processes more generally. And even when the cell would proceed in one particular direction, it must “choose” the exact point in the genetic sequence at which to begin. Different starting points can yield functionally distinct results. “Many studies focusing on single genes have shown that the choice of a specific transcription start site has critical roles during development and cell differentiation, and aberrations in . . . transcription start site use lead to various diseases including cancer, neuropsychiatric disorders, and developmental disorders”.8,,, The (protein) enzyme that transcribes DNA into RNA is RNA polymerase12. The enzyme certainly does not work alone, however, and its task is by no means cut-and-dried. To begin with, its critical interactions with various elements of the pre-initiation complex help determine whether and exactly where transcription will begin, if it is to begin at all. Then, after those “decisions” have been made, RNA polymerase moves along the double helix transcribing the sequence of genetic “letters” into the complementary sequence of an RNA. Throughout this productive journey, which is called elongation, the RNA polymerase still keeps good and necessary company. Certain co-activators modify it during its transit of a genetic locus, and these modifications not only enable transcription elongation to begin, but also provide binding sites for yet other proteins that will cooperate throughout the transcription journey.,,, Finally — and mirroring all the possibilities surrounding initiation of gene transcription — there are the issues relating to its termination. Again, they are far too many to mention here. Transcription may conclude at a more or less canonical terminus, or at an alternative terminus, or it may proceed altogether past the gene locus, even to the point of overlapping what, by usual definitions, would be regarded as a separate gene farther “downstream”. The cell has great flexibility in determining what, on any given occasion, counts as a gene, or transcriptional unit. The last part of the transcribed gene is generally non-protein-coding, but nevertheless contains great significance. Examining this region in a single gene, a research team recently identified “at least 35 distinct regulatory elements” to which other molecules can bind.13 Further regulatory potentials arise from yet more binding sites on the customized “tail” that the cell adds to the RNA immediately upon conclusion of its transcription. Proteins and other molecules that bind to the various regulatory elements of the non-protein-coding portion of the transcript do so in a context-sensitive manner, where cell and tissue type, phase of the cell cycle, developmental stage, location of the RNA within the cell, and environmental factors, both intra- and extra-cellular, may all play a role. These converging influences can change the stability of the RNA, change its localization within the cell, and change the efficiency of its translation into protein, among other possibilities.,,, What is generally considered the post-transcriptional modulation of gene expression actually begins during transcription proper. A prime example has to do with what happens partly as a result of the pauses during elongation. Cells don’t just passively accept the RNAs that emerge from the transcription process, but rather “snip and stitch” them via an elaborate procedure known as RNA splicing. It happens that the cutting out and knitting together of selected pieces typically begins before the RNA is fully transcribed, and the rhythm of pauses during elongation has an important influence upon which pieces form the mature transcript. This splicing operation, which is applied to nearly all human RNAs, is performed by the spliceosome, consisting of a few non-protein-coding RNAs and over 300 cooperating proteins, and is hardly less exacting in its requirements than, say, brain surgery. For the vast majority of human genes the operation can be performed in different ways, yielding distinct proteins (called isoforms) from a single RNA derived from a single DNA sequence. This is called alternative splicing, and it would be hard to find anything in human development, disease etiology, or normal functioning that is not dependent in one way or another on the effectiveness of this liberty the cell takes with its gene products. But RNA splicing is hardly the end of it. Through RNA editing the cell can add, delete, or substitute individual “letters” of the RNA sequence.15 Or, leaving the letters in place, the cell can chemically modify them in any of over one hundred different ways.16 ,,, Eventually, a protein-coding RNA needs to be translated into protein. This happens by means of large molecular complexes called “ribosomes”. Just as with gene transcription, there are many associated factors that must work together to bring about the initiation of translation, many that cooperate with the ribosome during translation, and yet others that play a role in modifying, localizing, or otherwise regulating the newly produced protein. The overall picture of gene expression is one of unsurveyable complexity in the service of remarkably effective living processes.,,, A decisive problem for the classical view of DNA is that “as cells differentiate and respond to stimuli in the human body, over one million different proteins are likely to be produced from less than 25,000 genes”.30 Functionally, in other words, you might say that we have over a million genes.,,, http://www.natureinstitute.org/txt/st/org/comm/ar/2015/genes_29.htm

So CR, if you took the time to read the preceding, do you still really, really, really, believe that Dawkins selfish gene metaphor is correct? and that genes are running the show in biology? And if you are sane enough to not believe that anymore, are you honest enough to admit that you were wrong in your 'selfish gene' presupposition? If not, why not? What has the selfish gene metaphor ever done for you except lead you down a primrose path of thinking yourself wise in molecular biology when in fact you were grossly ignorant of the astonishing complexity of molecular biology?

Genetics: Dawkins, redux - Nathaniel Comfort -Nature - 525, 184–185 (10 September 2015) Excerpt: A curious stasis underlies Dawkins's thought. His biomorphs are grounded in 1970s assumptions. Back then, with rare exceptions, each gene specified a protein and each protein was specified by a gene. The genome was a linear text — a parts list or computer program for making an organism —insulated from the environment, with the coding regions interspersed with “junk”. Today's genome is much more than a script: it is a dynamic, three-dimensional structure, highly responsive to its environment and almost fractally modular. Genes may be fragmentary, with far-flung chunks of DNA sequence mixed and matched in bewildering combinatorial arrays. A universe of regulatory and modulatory elements hides in the erstwhile junk. Genes cooperate, evolving together as units to produce traits. Many researchers continue to find selfish DNA a productive idea, but taking the longer view, the selfish gene per se is looking increasingly like a twentieth-century construct. http://www.nature.com/nature/journal/v525/n7568/full/525184a.html Revisiting the Central Dogma in the 21st Century - James A. Shapiro - 2009 Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112). http://shapiro.bsd.uchicago.edu/Shapiro2009.AnnNYAcadSciMS.RevisitingCentral%20Dogma.pdf

Also of interest from the preceding paper, on page 22, is a simplified list of the ‘epigenetic’ information flow in the cell that directly contradicts what was expected from the central dogma (Genetic Reductionism/modern synthesis model) of neo-Darwinism.

"It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works. All careful studies of mutagenesis find statistically significant non-random patterns” James Shapiro - Evolution: A View From The 21st Century - (Page 82)

And at the 10:30 minute mark of the following video, Dr. Trifonov states that the concept of the selfish gene 'inflicted an immense damage to biological sciences', for over 30 years:

Second, third, fourth… genetic codes - One spectacular case of code crowding - Edward N. Trifonov - video https://www.youtube.com/watch?v=fDB3fMCfk0E

So again CR, are you honest enough to follow the evidence where it leads? bornagain77

“I’m sure you are right to a certain degree, yet this following statement is the one of most interest to me… “Most of Scott’s genes did indeed return to normal after a brief time back here on Earth, but not all of them.” … It is that finding in particular that directly falsifies the “central dogma” of Darwinian evolution since its shows the organism controlling its DNA, not the DNA controlling the organism as is presupposed by Darwinists.”

Um.. And where does most of the knowledge of how to modulate DNA in a cell come from? Other knowledge, which takes the form of, you guessed it, knowledge laden genes. critical rationalist

A few things that might clear things up a little... There are not 1400 genes that remain differentially expressed in twins. Rather, 7% of those genes that were differentially expressed remain so. There are only a few hundred genes with apparently continued differential expression. We know these expression changes are statistically significant, but not how large they are. Gene expression can be quite sloppy, so minor changes in transcript abundance may have little physiological effect. It's a bit weird to ask how homeostasis can handle changes in gene expression. It's quite possible that the changes in gene expression are homeostasis. Physiological cues brought about by strange food, lack of weight-bearing exercise etc giving rise to changes in gene expression. Hard to see the challenge to evolutionary biology there. I agree with others the telomere result is the most interesting. But I can't see why this result is qualitatively different than the gene expression one. To lengthen telomeres, you just need to express more telomerase (as happens in cancer cells on earth). cornu

As to:

"There should, of course, be a physiological explanation …"

Seeing as Darwinian explanations don't even get out of the gate as to providing anything resembling a coherent explanation, (much less a testable one), that would be one avenue. But alas, Physiology, much like all of biology, is not a friend of Darwinian evolution:

"Physiology Is Rocking the Foundations of Evolutionary Biology": Another Peer-Reviewed Paper Takes Aim at Neo-Darwinism - Casey Luskin March 31, 2015 Excerpt: Noble doesn't mince words: "It is not only the standard 20th century views of molecular genetics that are in question. Evolutionary theory itself is already in a state of flux (Jablonka & Lamb, 2005; Noble, 2006, 2011; Beurton et al. 2008; Pigliucci & Muller, 2010; Gissis & Jablonka, 2011; Shapiro, 2011). In this article, I will show that all the central assumptions of the Modern Synthesis (often also called Neo-Darwinism) have been disproved." Noble then recounts those assumptions: (1) that "genetic change is random," (2) that "genetic change is gradual," (3) that "following genetic change, natural selection leads to particular gene variants (alleles) increasing in frequency within the population," and (4) that "inheritance of acquired characteristics is impossible." He then cites examples that refute each of those assumptions,,, He then proposes a new and radical model of biology called the "Integrative Synthesis," where genes don't run the show and all parts of an organism -- the genome, the cell, the body plan, everything -- is integrated. http://www.evolutionnews.org/2015/03/physiology_is_r094821.html Evolutionary dilemma The more we know about DNA, the tougher things get for modern Darwinism --- None other than the President of the International Union of Physiological Sciences, Professor Denis Noble (Oxford University), has presented a paper where he set out to show “that all the central assumptions of the Modern Synthesis (often also called Neo-Darwinism) have been disproved.” Noble says he hopes for a new theory of ‘evolution’ that will explain the evidence.2,,, https://creation.com/evolutionary-dilemma

Noble may hope for a "new theory of evolution" that will explain the evidence, but alas, since it is a unfalsifiable pseudoscience, Darwinian evolution will still go on in spite of the evidence. Just as it has always done since its inception. Nobel's mistake is that he thinks he is dealing with a science instead of a religion. bornagain77

Another possible avenue for research is to look at genetic changes caused by high pressures such as experienced by divers. We obviously did not evolve specifically to thrive under multiple atmospheres of pressure. But we know that we can survive for extended periods under such conditions. Do we experience changes in gene expression under high pressure? How quickly do they revert to “normal” when we are brought back to the surface. Allan Keith

Bob, it seems that I cannot get my point across. I am not a native English speaker, so this miscommunication may very well be due to my limited ability to express myself. Origenes

If evolution is true, if it can potentially explain what happens to ppl in space, then there should be a conceivable evolutionary explanation for why astronauts do not fall apart in space. Right?

Err, why? We haven't evolved in space. So I can't see an evolutionary explanation beyond "humans have evolved not to fall apart on earth". Of course, it's possible that humans don't fall apart in space because of intelligent design. i.e. humans have designed the space station to maintain human life.

Explanation for why Scott’s homeostasis is up to the task of handling a lot of weird gene change?

Who said it's weird? See Allan Keith's comment @ 15.

We are indeed talking past each other…. At no point did I ask why there would be a response to space. That is not my question Bob. It never was.

Well ,except for where you wrote "For clarity, it seems to me that a sudden change in 1400 genes poses a challenge for Kelly’s homeostasis." Bob O'H

Bob@

... given that we’ve not been into space before, I don’t see why there would be an evolutionary explanation.

"Why there would be ... "?? Are we talking past each other? If evolution is true, if it can potentially explain what happens to ppl in space, then there should be a conceivable evolutionary explanation for why astronauts do not fall apart in space. Right?

There should, of course, be a physiological explanation ...

Explanation for why Scott's homeostasis is up to the task of handling a lot of weird gene change?

... and that might lead to an explanation for why there would be a response to an environment similar to space.

We are indeed talking past each other.... At no point did I ask why there would be a response to space. That is not my question Bob. It never was. Origenes

Origenes, I agree that the lengthening of the telomeres, and then rapid shortening of them after landing, is the most interesting aspect. It would be interesting to see if the inverse is also seen; do the telomeres shorten when exposed to higher gravity and lengthen again to normal length when returned to normal gravity? I imagine that this could be tested by use of a specially designed centrifuge. But the big question is, what does this even mean? I certainly don't. Allan Keith

Otigenes - given that we've not been into space before, I don't see why there would be an evolutionary explanation. There should, of course, be a physiological explanation, and that might lead to an explanation for why there would be a response to an environment similar to space. But without knowing much more, I'm not sure we could say a great deal. BTW, telomeres aren't genes. They are stretches of repetitive DNA at the ends of chromosomes, which act as caps. Sort-of (vaguely) like the plastic/metal things on the ends of boot laces that stop them from fraying. Bob O'H

Allan Keith: All of these symptoms also occur to people on earth, just not typical at the same time.

If you are correct, if all space-gene-changes also occur on earth, then the evolutionary narrative lives another day. However, this is not what the article suggests. For instance:

Scott’s telomeres (endcaps of chromosomes that shorten as one ages) actually became significantly longer in space.

suggests some unknown (extraterrestrial?) gene change. Origenes

Bob: No. What I mans was that the environment one finds oneself in triggers a signal in the cell(s) that causes gene expression to change.

Okay. But that leaves the question "what can be the evolutionary explanation for the fact that Scott Kelly’s homeostasis holds?" unanswered, right? For clarity, it seems to me that a sudden change in 1400 genes poses a challenge for Kelly's homeostasis. Maybe I did not make that clear. I would also like to know how many genes undergo short term changes. Unfortunately the article doesn't say. A lot of change would trigger the question: why do astronauts not fall apart in space? Origenes