Less Junk, More ID Predictions Confirmed

_{December 7, 2015

Intelligent Design}

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It is simply a matter of time before the Darwinists (I know they prefer “evolutionary biologists,” but evolution is not evolution without “Origin of Species”) will have to give up.

Every day in labs around the world, more and more function is being found for “junk” DNA. This is a two-fold problem for the Darwinists.

The first problem is that this is NOT what they predicted, even though, quite cavalierly, they say then never said any such thing. But, of course, we know better.

Second, there’s the problem of “de novo” genes, and the solution for this is to look to so-called “junk” DNA as a potential template for these ‘new’ genes. If “junk” DNA is ‘neutral,’ then no problem; but if it has a function, then the nursery from which they can harvest “de novo” genes from within the genome lessens. As I say, it’s a matter of time.

From Phys.Org we have a snippet from a news summary:

In the first study to run a genome-wide analysis of Short Tandem Repeats (STRs) in gene expression, a large team of computational geneticists led by investigators from Columbia Engineering and the New York Genome Center have shown that STRs, thought to be just neutral, or “junk,” actually play an important role in regulating gene expression. The work, which uncovers a new class of genetic variants that modulate gene expression, is published on Nature Genetics’s Advance Online Publication website on December 7.

Erlich’s study looked at Short Tandem Repeats (STRs), variants that create what look like typos: stutter vs. stututututututter. Most researchers, assuming that STRs were neutral, dismissed them as not important. In addition, these variants are extremely hard to study. “They look so different to analysis algorithms,” Erlich notes, “that they just usually classify them as noise and skip these positions.”

And, revealing a mechanism I have long suspected could be the true purpose, or function, of these repeated elements, they say:

Erlich used a multitude of statistical genetic and integrative genomics analyses to reveal that STRs have a function: they act like springs or knobs that can expand and contract, and fine-tune the nearby gene expression. Different lengths correspond to different tensions of the spring and can control gene expression and disease traits.

Comments

jw777: All pertinent and outspoken evolutionary biologists and thinkers in the Darwin and NeoDarwin camp predicted (rightly per their worldview) that there would be endless swaths of useless genetic data. Darwinists generally rejected the idea of endless swaths of useless genetic data. jw777: PREDICTION IS A ZERO SUM GAME. Which is why there are few strict darwinists left in the biological sciences.Zachriel_{December 9, 2015
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JW77 Where is the evidence that most of the (human I guess) genome is not junk?wd400_{December 8, 2015
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Mung @21
I just love the role reversal. It’s just a matter of time until we find all those missing links. It’s just a matter of time until we find function for all that junk.
Good observation! Darwinism of the gaps? :)Dionisio_{December 8, 2015
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Although I can understand why wd400 and other 0ist apologists are proffering equivocations, the fact remains that in the scientific game PREDICTION IS A ZERO SUM GAME. Prediction either does or doesn't come true. End of discussion. All pertinent and outspoken evolutionary biologists and thinkers in the Darwin and NeoDarwin camp predicted (rightly per their worldview) that there would be endless swaths of useless genetic data. All pertinent and outspoken scientists and thinkers in the intelligent design and creationist camps predicted "junk DNA" would have purpose, function and often immediately con temporarily so. One group lost. One group won. Come to the table with whatever apologetics and equivocations you like, but this is a simple and immutable historical fact that will never go away. And it's only getting worse for the last few dinosaurs trying to hold onto the great hope of Dawkins and his ilk. Luddites.jw777_{December 8, 2015
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wd400, references please. (and sequence comparisons that assume common descent do not count as 'tests')bornagain_{December 8, 2015
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Darwinists should ask themselves WHY they thought these things were just neutral or “junk” and reflect a bit on that.
Well, the main reason we think most STRs evolve neutrally is that the idea they are under selection has repeatedly been tested and found not found to be true (for most loci). This hasn't stopped anyone studying the minority of loci that do have appreciable effects -- STR instability is a well-understood phenomenon in some cancers and long been known to be responsible for neurological diseases including Huntington's. In this study only a small proportion of the STRs studied had an appreciable phenotype, and, of course, having a phenotype is different than being non-neutral.wd400_{December 8, 2015
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I just love the role reversal. It's just a matter of time until we find all those missing links. It's just a matter of time until we find function for all that junk. :)Mung_{December 8, 2015
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Alicia Cartelli:
Am I missing something here?
Isn't that obvious?Mung_{December 8, 2015
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Bob O'H:
so we’ve moved far beyond what Darwin proposed.
Not really as Darwin didn't have any supporting evidence and neither do you.Virgil Cain_{December 8, 2015
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STRs, thought to be just neutral, or “junk,” actually play an important role in regulating gene expression.
Darwinists should ask themselves WHY they thought these things were just neutral or "junk" and reflect a bit on that. Why? And what does this have to say about the paradigm that produced that prediction? Hmm. If this stuff is largely NOT junk, that too needs to be explained. Why isn't it? The junk idea makes a lot of sense from the Darwinian viewpoint. But if it is not junk, why not? Can the Darwinian paradigm sufficiently explain that? I agree with the OP. It's just a matter of time! It will obviously take still a long time to investigate each and every part of the genome, but the trend is clear and it is NOT encouraging for Darwinists.tjguy_{December 8, 2015
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Bob O'H you state: "More seriously, evolutionary biology wouldn’t be evolutionary biology without what happened after OoS (e.g. population genetics), so we’ve moved far beyond what Darwin proposed." Population genetics has done nothing for Darwinian evolution save for to prove it is false from yet another mathematical angle and remove Natural Selection as a supposed major player in biological innovation. Waiting Longer for Two Mutations - Michael J. Behe Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that 'for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years' (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless "using their model" gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model.,,, The difficulty with models such as Durrett and Schmidt’s is that their biological relevance is often uncertain, and unknown factors that are quite important to cellular evolution may be unintentionally left out of the model. That is why experimental or observational data on the evolution of microbes such as P. falciparum are invaluable,,, http://www.discovery.org/a/9461 More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012 Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population. You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect. Facing Facts But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes. https://uncommondescent.com/intelligent-design/more-from-ann-gauger-on-why-humans-didnt-happen-the-way-darwin-said/ Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory - 2008 Abstract: Evolutionary genetic theory has a series of apparent “fatal flaws” which are well known to population geneticists, but which have not been effectively communicated to other scientists or the public. These fatal flaws have been recognized by leaders in the field for many decades—based upon logic and mathematical formulations. However population geneticists have generally been very reluctant to openly acknowledge these theoretical problems, and a cloud of confusion has come to surround each issue. Numerical simulation provides a definitive tool for empirically testing the reality of these fatal flaws and can resolve the confusion. The program Mendel’s Accountant (Mendel) was developed for this purpose, and it is the first biologically-realistic forward-time population genetics numerical simulation program. This new program is a powerful research and teaching tool. When any reasonable set of biological parameters are used, Mendel provides overwhelming empirical evidence that all of the “fatal flaws” inherent in evolutionary genetic theory are real. This leaves evolutionary genetic theory effectively falsified—with a degree of certainty which should satisfy any reasonable and open-minded person. http://www.icr.org/i/pdf/technical/Using-Numerical-Simulation-to-Test-the-Validity-of-Neo-Darwinian-Theory.pdf 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/ Using Numerical Simulation to Better Understand Fixation Rates, and Establishment of a New Principle - "Haldane's Ratchet" - Christopher L. Rupe and John C. Sanford - 2013 Excerpt: We then perform large-scale experiments to examine the feasibility of the ape-to-man scenario over a six million year period. We analyze neutral and beneficial fixations separately (realistic rates of deleterious mutations could not be studied in deep time due to extinction). Using realistic parameter settings we only observe a few hundred selection-induced beneficial fixations after 300,000 generations (6 million years). Even when using highly optimal parameter settings (i.e., favorable for fixation of beneficials), we only see a few thousand selection-induced fixations. This is significant because the ape-to-man scenario requires tens of millions of selective nucleotide substitutions in the human lineage. Our empirically-determined rates of beneficial fixation are in general agreement with the fixation rate estimates derived by Haldane and ReMine using their mathematical analyses. We have therefore independently demonstrated that the findings of Haldane and ReMine are for the most part correct, and that the fundamental evolutionary problem historically known as "Haldane's Dilemma" is very real. Previous analyses have focused exclusively on beneficial mutations. When deleterious mutations were included in our simulations, using a realistic ratio of beneficial to deleterious mutation rate, deleterious fixations vastly outnumbered beneficial fixations. Because of this, the net effect of mutation fixation should clearly create a ratchet-type mechanism which should cause continuous loss of information and decline in the size of the functional genome. We name this phenomenon "Haldane's Ratchet". http://media.wix.com/ugd/a704d4_47bcf08eda0e4926a44a8ac9cbfa9c20.pdf Haldane’s Dilemma Excerpt: Haldane was the first to recognize there was a cost to selection which limited what it realistically could be expected to do. He did not fully realize that his thinking would create major problems for evolutionary theory. He calculated that in man it would take 6 million years to fix just 1,000 mutations (assuming 20 years per generation).,,, Man and chimp differ by at least 150 million nucleotides representing at least 40 million hypothetical mutations (Britten, 2002). So if man evolved from a chimp-like creature, then during that process there were at least 20 million mutations fixed within the human lineage (40 million divided by 2), yet natural selection could only have selected for 1,000 of those. All the rest would have had to been fixed by random drift – creating millions of nearly-neutral deleterious mutations. This would not just have made us inferior to our chimp-like ancestors – it surely would have killed us. Since Haldane’s dilemma there have been a number of efforts to sweep the problem under the rug, but the problem is still exactly the same. ReMine (1993, 2005) has extensively reviewed the problem, and has analyzed it using an entirely different mathematical formulation – but has obtained identical results. John Sanford PhD. – “Genetic Entropy and The Mystery of the Genome” – pg. 159-160 Kimura’s Quandary Excerpt: Kimura realized that Haldane was correct,,, He developed his neutral theory in response to this overwhelming evolutionary problem. Paradoxically, his theory led him to believe that most mutations are unselectable, and therefore,,, most ‘evolution’ must be independent of selection! Because he was totally committed to the primary axiom (neo-Darwinism), Kimura apparently never considered his cost arguments could most rationally be used to argue against the Axiom’s (neo-Darwinism’s) very validity. John Sanford PhD. – “Genetic Entropy and The Mystery of the Genome” – pg. 161 – 162bornagain_{December 8, 2015
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It is simply a matter of time before the Darwinists (I know they prefer “evolutionary biologists,” but evolution is not evolution without “Origin of Species”) will have to give up.
Woohoo! ID wouldn't be ID without Biblical Creationism, so now we can call you all creationists! More seriously, evolutionary biology wouldn't be evolutionary biology without what happened after OoS (e.g. population genetics), so we've moved far beyond what Darwin proposed.Bob O'H_{December 8, 2015
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of related note to this:
Podcast – Richard Sternberg PhD – On Human Origins: Is Our Genome Full of Junk DNA? Part 2 (Major Differences in higher level chromosome spatial organization between even supposedly closely related species) http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-2/
and this:
Tissue-specific spatial organization of genomes – 2004 Excerpt: Using two-dimensional and three-dimensional fluorescence in situ hybridization we have carried out a systematic analysis of the spatial positioning of a subset of mouse chromosomes in several tissues. We show that chromosomes exhibit tissue-specific organization. Chromosomes are distributed tissue-specifically with respect to their position relative to the center of the nucleus and also relative to each other. Subsets of chromosomes form distinct types of spatial clusters in different tissues and the relative distance between chromosome pairs varies among tissues. Consistent with the notion that nonrandom spatial proximity is functionally relevant in determining the outcome of chromosome translocation events, we find a correlation between tissue-specific spatial proximity and tissue-specific translocation prevalence. Conclusion: Our results demonstrate that the spatial organization of genomes is tissue-specific and point to a role for tissue-specific spatial genome organization in the formation of recurrent chromosome arrangements among tissues. http://genomebiology.com/content/5/7/R44
is this:
Mouse gene expression reveals “widespread differences” from humans - Nov. 22, 2014 Excerpt: an international group of researchers has found powerful clues to why certain processes and systems in the mouse — such as the immune system, metabolism and stress response — are so different from those in people.,,, Mice are widely used to model human metabolism, disease, and drug response. But results published today (November 17) in PNAS reveal widespread differences between human and mouse gene expression, both in protein-coding and noncoding genes,,, Michael Snyder of Stanford University and his colleagues compared how genes are expressed in 15 different human and mouse tissues, including brain, heart, liver, and kidney. They found that gene expression patterns clustered by species rather than tissues. For example, gene expression in a mouse liver more closely resembled the patterns observed in a mouse heart than those observed in a human liver. https://uncommondescent.com/genetics/mouse-gene-expression-reveals-widespread-differences-from-humans/
bornagain_{December 7, 2015
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What Is The Genome? It's Certainly Not Junk! - Dr. Robert Carter - video - (Notes in video description) http://www.metacafe.com/w/8905583 Comparing genomes to computer operating systems - Van - May 2010 Excerpt: we present a comparison between the transcriptional regulatory network of a well-studied bacterium (Escherichia coli) and the call graph of a canonical OS (Linux) in terms of topology,,, http://www.ncbi.nlm.nih.gov/pubmed/20439753 “Millions of DNA Switches That Power Human Genome’s Operating System Are Discovered.” - Sept. 2012 http://www.sciencedaily.com/releases/2012/09/120905135326.htm Bits of Mystery DNA, Far From ‘Junk,’ Play Crucial Role - September 2012 Excerpt: The system, though, is stunningly complex, with many redundancies. Just the idea of so many switches was almost incomprehensible, Dr. Bernstein said. There also is a sort of DNA wiring system that is almost inconceivably intricate. “It is like opening a wiring closet and seeing a hairball of wires,” said Mark Gerstein, an Encode researcher from Yale. “We tried to unravel this hairball and make it interpretable.” There is another sort of hairball as well: the complex three-dimensional structure of DNA. Human DNA is such a long strand — about 10 feet of DNA stuffed into a microscopic nucleus of a cell — that it fits only because it is tightly wound and coiled around itself. When they looked at the three-dimensional structure — the hairball — Encode researchers discovered that small segments of dark-matter DNA are often quite close to genes they control. In the past, when they analyzed only the uncoiled length of DNA, those controlling regions appeared to be far from the genes they affect. http://www.nytimes.com/2012/09/06/science/far-from-junk-dna-dark-matter-proves-crucial-to-health.html?_r=1&pagewanted=all News from Epigenetics - Dec. 21, 2012 Excerpt: They are organized into “nonrandom spatial clustering” the authors dub“rich clubs,” communities and spokes. This large-scale organization helps repress mutations among vital genes, and “shapes functionally compartmentalized and error-tolerant transcriptional regulation of human genome in three dimensions.” per crevo There’s a Mystery Machine That Sculpts the Human Genome -Oct 20, 2015 Excerpt: Consider that the human genome is longer than the average human. It consists of around two meters of DNA, which must somehow fit into cells, whose nuclei are about 200,000 times narrower. So it folds. And it folds in such a way that any given stretch can be easily unfolded, so the genes within it can be read and used. Knots are verboten,,, In the 1970s, biochemists showed that this feat of extreme origami begins when DNA is wrapped around proteins called histones, creating what looks like a string of beads. This reduces the packing problem, but doesn’t come close to solving it. The wrapped DNA must be folded and twisted in ever more complicated (and as yet unknown) ways. Eventually, it forms large loops.,,, “That was a total bombshell,” says student Suhas Rao who worked on the project. He, like many others, had assumed that loops form when two stretches of free-floating DNA randomly find each other and are fastened by a pair of CTCF proteins. But that can’t be right. If it was, the CTCF landing sequences would align in all four possible orientations, rather than the very specific one that Rao saw in his data. The loops must be forming in a completely different way, one that’s deliberate and controlled. ,,, “This is an important milestone in understanding the three dimensional structure of chromosomes, but like most great papers, it raises more questions than it provides answers,” http://www.theatlantic.com/science/archive/2015/10/theres-a-mystery-machine-that-sculpts-the-human-genome/411199/ The Extreme Complexity Of Genes – Dr. Raymond G. Bohlin - video http://www.metacafe.com/watch/8593991/ Design In DNA – Alternative Splicing, Duons, and Dual coding genes – video (5:05 minute mark) http://www.youtube.com/watch?v=Bm67oXKtH3s#t=305 Landscape of transcription in human cells – Sept. 6, 2012 Excerpt: Here we report evidence that three-quarters of the human genome is capable of being transcribed, as well as observations about the range and levels of expression, localization, processing fates, regulatory regions and modifications of almost all currently annotated and thousands of previously unannotated RNAs. These observations, taken together, prompt a redefinition of the concept of a gene.,,, Isoform expression by a gene does not follow a minimalistic expression strategy, resulting in a tendency for genes to express many isoforms simultaneously, with a plateau at about 10–12 expressed isoforms per gene per cell line. http://www.nature.com/nature/journal/v489/n7414/full/nature11233.html
Verse and Music:
Psalm 139:14 I will praise thee; for I am fearfully and wonderfully made: marvellous are thy works; and that my soul knoweth right well. Johnny Cash - Ain't No Grave http://www.youtube.com/watch?v=o0MIFHLIzZY
bornagain_{December 7, 2015
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Perhaps it would help Darwinists out immensely if they could prove that unguided material processes can produce ANY non-trivial functionality before they start labeling everything that they don't understand in the genome as 'junk'? After all, would not that be the proper 'scientific' thing to do? As far as the science is concerned, it is simply sheer insanity for hard-core Darwinists to insist that most of the genome is junk when they have not even experimentally demonstrated the origin of a single gene/protein by unguided material processes. Much less demonstrated the origin of the absolutely jaw-dropping complexity we do witness in the genome that is in fact regulating the genes/proteins.
Will we ever… reveal all the secrets of life from DNA? - Nov. 2, 2012 Excerpt: our metaphors let us down. Science writers like to compare the genome to a textbook or a blueprint. That conveys the fact that it stores information, but glosses over its buzzing, dynamic nature – proteins docking on and off to control the activity of genes, huge stretches of DNA that fold and unfold to reveal or hide their sequences,,, jumping genes that copy themselves and hop throughout the genome... None of our information stores – not sheet music, not recipe books – are this intricate. http://www.bbc.com/future/story/20121102-will-we-ever-crack-lifes-code/1 Complex grammar of the genomic language - November 9, 2015 Excerpt: The 'grammar' of the human genetic code is more complex than that of even the most intricately constructed spoken languages in the world. The findings explain why the human genome is so difficult to decipher --,,, ,,, in their recent study in Nature, the Taipale team examines the binding preferences of pairs of transcription factors, and systematically maps the compound DNA words they bind to. Their analysis reveals that the grammar of the genetic code is much more complex than that of even the most complex human languages. Instead of simply joining two words together by deleting a space, the individual words that are joined together in compound DNA words are altered, leading to a large number of completely new words. http://www.sciencedaily.com/releases/2015/11/151109140252.htm Shoddy Engineering or Intelligent Design? Case of the Mouse's Eye - April 2009 Excerpt: -- The (entire) nuclear genome is thus transformed into an optical device that is designed to assist in the capturing of photons. This chromatin-based convex (focusing) lens is so well constructed that it still works when lattices of rod cells are made to be disordered. Normal cell nuclei actually scatter light. -- So the next time someone tells you that it “strains credulity” to think that more than a few pieces of “junk DNA” could be functional in the cell - remind them of the rod cell nuclei of the humble mouse. http://www.evolutionnews.org/2009/04/shoddy_engineering_or_intellig.html Tissue-specific spatial organization of genomes - 2004 Excerpt: Using two-dimensional and three-dimensional fluorescence in situ hybridization we have carried out a systematic analysis of the spatial positioning of a subset of mouse chromosomes in several tissues. We show that chromosomes exhibit tissue-specific organization. Chromosomes are distributed tissue-specifically with respect to their position relative to the center of the nucleus and also relative to each other. Subsets of chromosomes form distinct types of spatial clusters in different tissues and the relative distance between chromosome pairs varies among tissues. Consistent with the notion that nonrandom spatial proximity is functionally relevant in determining the outcome of chromosome translocation events, we find a correlation between tissue-specific spatial proximity and tissue-specific translocation prevalence. Conclusion: Our results demonstrate that the spatial organization of genomes is tissue-specific and point to a role for tissue-specific spatial genome organization in the formation of recurrent chromosome arrangements among tissues. http://genomebiology.com/content/5/7/R44 Scientists' 3-D View of Genes-at-Work Is Paradigm Shift in Genetics - Dec. 2009 Excerpt: Highly coordinated chromosomal choreography leads genes and the sequences controlling them, which are often positioned huge distances apart on chromosomes, to these 'hot spots'. Once close together within the same transcription factory, genes get switched on (a process called transcription) at an appropriate level at the right time in a specific cell type. This is the first demonstration that genes encoding proteins with related physiological role visit the same factory. http://www.sciencedaily.com/releases/2009/12/091215160649.htm “Three-Dimensional Connections Across the Genome“ Keith Dunaway - ENCODE 2012 Excerpt: These analyses portray a complex landscape of long-range gene-element connectivity across ranges of hundreds of kb to several Mb, including interactions among unrelated genes (Supplementary Figure Y1). Furthermore, in the 5C results, 50-60% of long-range interactions occurred in only one of the four cell lines, indicative of a high degree of tissue specificity for gene-element connectivity http://www.nature.com/encode/threads/three-dimensional-connections-across-the-genome Large-Scale Functional Organization of Long-Range Chromatin Interaction Networks - 25 October 2012 Excerpt Introduction: Long-range chromatin interactions are pervasive in the human genome and serve to regulate gene expression.,, Proximity ligation in combination with next-generation sequencing has recently enabled us to explore genome-wide spatial crosstalk in the chromatin.,,, The observation of most interest was that interacting promoters not only correlate with gene coexpression, but can also regulate each other’s transcriptional states, which blurs the traditional definitions of gene-regulatory elements in the genome. These observations support the notion of a chromatin interactome encompassing a dense repertoire of regulatory elements for transcriptional regulation. http://www.cell.com/cell-reports/abstract/S2211-1247%2812%2900326-9?switch=standard Human Nucleome Reveals Amazing 4D World - Jeffrey P. Tomkins, Ph.D. - July 27, 2015 Excerpt: As if three dimensions were not enough, the researchers repeated these experiments across multiple time points in response to the body's day/night time-keeping system—called a circadian clock—adding the fourth dimension of time to the study. Amazingly, they discovered thousands of genes across the genome dynamically and precisely regulated by the body's internal clock. This stunning orchestration of complex genetic activity occurs across the 3D genome. The researchers wrote, "Genomic movements in 3D space provide a geometric picture of gene regulation in the context of circadian clocks, one that may give insight into the mechanisms regulating biological time."1 Not only are thousands of genes coordinately regulated together in 3D space in a precise manner according to cell type and relevant physiological processes, but they also function within the context of time, the fourth dimension, in a wondrously precise genetic dance. These types of biological systems are incredibly complicated and our understanding of them is only beginning. The complexity is astounding and utterly defies the failed evolutionary paradigm that this all somehow developed through random purposeless processes. http://www.icr.org/article/8840
bornagain_{December 7, 2015
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PaV [#11 addendum] In the Discussion section of that paper they wrote this:
We hypothesize that there are more eSTRs to find in the genome. We envision that recent advancements in sequencing technologies will further expand the catalog of eSTRs. Regardless of the technical method, our results suggest that such efforts might reveal exciting biology beyond that observed through the prism of traditional point mutations.
All that said, the presence of a significant proportion of DNA without known functionality, which may include parts that indeed don't have any functionality at all, should not surprise anyone. Had humans stayed in Eden, that would not have been an issue. But that first privileged couple fumbled it. We know what happened after that. The whole world is full of garbage (including myself). All creation is groaning. The good news is that all this will eventually disappear. A new Heaven and a new Earth will replace it. And the forgiven sinners through saving faith in the Lord of lords and King of kings will be able to sing hallelujah forever and ever. :) The rest will be somewhere else, eternally away from their Maker, singing Sinatra's hit song "I did it my way". :)Dionisio_{December 7, 2015
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PaV In the Discussion section of that paper they wrote this:
We hypothesize that there are more eSTRs to find in the genome. We envision that recent advancements in sequencing technologies will further expand the catalog of eSTRs. Regardless of the technical method, our results suggest that such efforts might reveal exciting biology beyond that observed through the prism of traditional point mutations.
All that said, the presence of a significant proportion of DNA without known functionality, which may include parts that indeed don't have any functionality at all, should not surprise anyone. Had humans stayed in Eden, that would not have been an issue. But that first privileged couple fumbled it. We know what happened after that. The whole world is full of garbage (including myself). All creation is groaning. The good news is that all this will eventually disappear. A new Heaven and a new Earth will replace it. :)Dionisio_{December 7, 2015
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PaV Interesting OP. Thank you. BTW, the actual article is behind a paywall: http://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3461.html But maybe the full PDF is available here: http://biorxiv.org/content/early/2015/04/02/017459.full.pdf or from the 'download PDF' link here: http://biorxiv.org/content/early/2015/04/02/017459Dionisio_{December 7, 2015
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bFast @4
If biologists had been listening to experts in other fields, they would have suspected it too. They would have figured out this relationship a long time ago.
Apparently some of them are doing that lately. They form multidisciplinary teams. I think there was one of those at Stanford University working on cell polarity in Drosophila, where the team leader was a lady who as far as I recall introduced herself as an electrical engineer specialized in control systems. Also, at some universities they have computer scientists working along the biologists in leading-edge research. But I agree with you that they should have done that much earlier. Your software development experience gives you an advantage when looking at the unending functional complexity (gpuccio's term) of the biological systems. Definitely you are better prepared to look at all that complex complexity from a different perspective and with a different attitude. For that reason you can ask questions about functional details that some scientists might not even notice.Dionisio_{December 7, 2015
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Some SINEs and LINEs drive expression of genes or do some other regulatory role (as has been known for a long time). Conflation between this fact and the idea all copies or SINEs and LINEs is required is a common mistake made by junk DNA skeptics.wd400_{December 7, 2015
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SINEs and LINEs have function?Alicia Cartelli_{December 7, 2015
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If ever there was a target for "junk" DNA, SINES and LINES would fit the bill. But, no, it has function. It's just a matter of time.PaV_{December 7, 2015
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Of semi-related note:
Podcast: Richard Sternberg PhD - " On Human Origins: Is Our Genome Full of Junk DNA? part 1 http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna/ Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 2 (Major Differences in higher level chromosome spatial organization between even supposedly closely related species) http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-2/ Podcast: Richard Sternberg PhD - " On Human Origins: Is Our Genome Full of Junk DNA? Part 3 http://intelligentdesign.podomatic.com/entry/2014-11-17T14_14_33-08_00 Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 4 http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-4/
In the following podcast, Dr. Sternberg’s emphasis is on ENCODE research, and how that research overturned the ‘central’ importance of the gene as a unit of inheritance. As well he reflects on how that loss of the term ‘gene’ as an accurate description in biology completely undermines the modern synthesis, (i.e. central dogma), of neo-Darwinism as a rational explanation for biology.
Podcast - Richard Sternberg PhD - On Human Origins: Is Our Genome Full of Junk DNA? Part 5 http://www.discovery.org/multimedia/audio/2014/11/on-human-origins-is-our-genome-full-of-junk-dna-pt-5/
bornagain_{December 7, 2015
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"Different lengths correspond to different tensions of the spring and can control" As a software developer, I have been looking for this phenomenon for a long time. We, as software developers, routinely produce numeric tunables, parameters, to allow the end user to get what (s)he wants. (For example, on the photocopier we have a lighter-darker slide.) The first time I heard of STRs, I wondered if that was their role. If biologists had been listening to experts in other fields, they would have suspected it too. They would have figured out this relationship a long time ago.bFast_{December 7, 2015
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...or ~2% what's considered mostly junk, and amounts to ~2--3% of the human genome...wd400_{December 7, 2015
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So by learning how a small fraction of what's considered junk DNA may play a role in evolution, this means that evolutionary biologists have to "give-up?" Am I missing something here?Alicia Cartelli_{December 7, 2015
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"It is simply a matter of time before the Darwinists (I know they prefer “evolutionary biologists,” but evolution is not evolution without “Origin of Species”) will have to give up." Actually, as far as I can tell, this is the typical Darwinian attitude towards the overwhelming evidence against them: The Last Great Act Of Defiance http://i1.cpcache.com/product_zoom/197401392/last_great_act_of_defiance_womens_plus_size_vnec.jpg?color=Black&height=460&width=460&padToSquare=true In other words, the typical Darwinists, as far as I can tell, would rather die a gruesome death than admit that Intelligence had anything to do with life on earth.bornagain_{December 7, 2015
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