Nature Reviews Genetics article admits that junk DNA has been “prematurely dismissed”

So 'junk' DNA a.k.a. ''we make **** up as we go along / typical evolutionary mindset / saying we do not know is forbidden'' regulatory properties are, after all, important. But they knew it, of course. :) We never said 'junk'! Tumor-driving mutations discovered in the under-explored regions of the cancer genome "Looking into the non-coding genome is really important because these vast sections regulate our genes and can switch them on and off. Mutations in these regions can cause these regulatory switches to act abnormally and potentially cause—or advance—cancer," says Helen Zhu, student at OICR and co-first author of the study. https://m.medicalxpress.com/news/2020-01-tumor-driving-mutations-under-explored-regions-cancer.html Truthfreedom

Bob @ 21. I mis-read; never mind. EDTA

Evolutionists, beware before calling something 'useless/junk'. Will you ever learn? 'Tonsils are small organs in the back of the throat. As part of the lymphatic system, they play an important role in the health of the body. Tonsils were once thought to be a useless part made obsolete by evolution. When bothered by an infection, doctors once prescribed the removal of the tonsils through a tonsillectomy. These small organs are actually quite useful, though' 'Though small and seemingly useless, tonsils have several uses. The tonsils prevent foreign objects from slipping into the lungs. Think of them as goalies for the throat. They also filter bacteria and viruses. On top of all that, they produce white blood cells and antibodies, according to the Mayo Clinic'. 'According to the American Academy of Otolaryngology, these bumps on the back of the throat are the "first line of defense as part of the immune system." For example, tonsils sample bacteria and viruses entering the body through the mouth or nose and flush them using lymph. Lymph is a clear and colorless fluid; the name comes from the Latin word lympha, which means "connected to water," according to the National Lymphadema Network". https://www.google.com/amp/s/www.livescience.com/amp/62447-tonsils.html Truthfreedom

EDTA - eh? Where did anyone say that intron loss was being used as evidence for evolution? Bob O'H

Bob O'H @ 11, And a thanks to BA77 for bring out the point I was leading to: if one has to assume common descent in order to conclude that introns are being lost, then the claim of introns being lost cannot be used as evidence for evolution: circular reasoning. EDTA

Sev @ 16. The improved efficiency would be in the cell replication process. If the vast majority of your DNA does not have to be copied into every daughter cell, every time, then the process requires much less energy and matter, i.e. occurs more efficiently. This would, of course, affect more than your brain since all your cells have the same DNA load - information to pass on to their daughters. Fasteddious

"Saved By Junk DNA: Vital Role In The Evolution Of Human Genome". 'Stretches of DNA previously believed to be useless 'junk' DNA play a vital role in the evolution of our genome, researchers have now shown. They found that unstable pieces of 'junk' DNA help tuning gene activity and enable organisms to quickly adapt to changes in their environments. https://www.sciencedaily.com/releases/2009/05/090528203730.htm Truthfreedom

@ Seversky: 'The point about “junk DNA” is that it’s assumed to be neither good nor bad. It could be removed without affecting the organism one way or the other. Cells would not become more or less efficient, they would just chug along the way they are'. Wrong. 'In a paper published in Nature Genetics, a team of German and American researchers has now shown that retrotranspons play a surprising and significant role in the development of embyros. The researchers looked at a kind of retrotransposon known as LINE1 elements, which were known to be involved early in the process of embryo creation. These elements are “highly expressed” in that phase, which means that they are read by the cellular machinery in order to produce RNA. By blocking or promoting the reading of the LINE1 elements at the two-cell stage of development in mouse embryos, the team found that too much or too little expression made development stop'. No development = no cells 'chugging along'. https://cosmosmagazine.com/biology/junk-dna-plays-a-vital-role-in-embryo-development Truthfreedom

Fasteddious @ 5

OK Sev, why don’t you put your genome where your mouth is: how much of your DNA do you want to get rid of as “junk”? Just think, if 90, or 50 or even 20% of your genome is really useless junk, then you don’t need it. Your cells would be more efficient without all that junk, right?

Wrong. The point about "junk DNA" is that it's assumed to be neither good nor bad. It could be removed without affecting the organism one way or the other. Cells would not become more or less efficient, they would just chug along the way they are. If neuroscientists could reliably identify the DNA that has no useful function then I would have no objection in principle to having it removed but why undergo the risks of neurosurgery to remove something that is not doing anything one way or the other? Seversky

Earth to Bob O'H- Your side cannot explain the existence of introns. You have nothing that can explain gene editing and splicing. So please, get a grip and buy a vowel. ET

'Junk DNA’ plays a vital role in embryo development': 'Strings of seemingly nonsense DNA play a surprising structural role in the early development of embryos, writes Michael Lucy. In mammals, almost half of the genome is made of repetitive stretches of DNA known as retrotransposons whose purpose has baffled scientists. Historically this genetic code has been known as ‘junk DNA’, though in recent years it has become clear that it is anything but disposable. In a paper published in Nature Genetics, a team of German and American researchers has now shown that retrotranspons play a surprising and significant role in the development of embryos'. https://cosmosmagazine.com/biology/junk-dna-plays-a-vital-role-in-embryo-development Truthfreedom

'But in the past few years, the tide has shifted within the field. Recent studies have revealed a wealth of new pieces of noncoding DNA that do seem to be as important to our survival as our more familiar genes. Many of them may encode molecules that help guide our development from a fertilized egg to a healthy adult, for example. If these pieces of noncoding DNA become damaged, we may suffer devastating consequences like brain damage or cancer, depending on what pieces are affected. Large-scale surveys of the genome have led a number of researchers to expect that the human genome will turn out to be even more full of activity than previously thought. In January, Francis Collins, the director of the National Institutes of Health, made a comment that revealed just how far the consensus has moved. At a health care conference in San Francisco, an audience member asked him about junk DNA. “We don’t use that term anymore,” Collins replied. “It was pretty much a case of hubris to imagine that we could dispense with any part of the genome — as if we knew enough to say it wasn’t functional.” Most of the DNA that scientists once thought was just taking up space in the genome, Collins said, “turns out to be doing stuff.” For Gregory and a group of like-minded biologists, this idea is not just preposterous but also perilous, something that could yield bad science. The turn against the notion of junk DNA, they argue, is based on overinterpretations of wispy evidence and a willful ignorance of years of solid research on the genome. They’ve challenged their opponents face to face at scientific meetings. They’ve written detailed critiques in biology journals.' https://www.google.com/amp/s/www.nytimes.com/2015/03/08/magazine/is-most-of-our-dna-garbage.amp.html Truthfreedom

Bob O'Hara claims that

We know that introns have been lost in yeast because the genes of related species have lots of introns.

Translation, they simply assumed that common descent (their unproven hypothesis) was true. Small problem with their unwarranted assumption of common descent, They have no empirical evidence that the transformation of one species of yeast into another species of yeast is remotely feasible. For example, as "one (evolutionist) explained: “We are trying to figure out the phylogenetic relationships of 1.8 million species and can’t even sort out 20 yeast.”

Here Are Those Incongruent Trees From the Yeast Genome - Case Study - Cornelius Hunter - June 2013 Excerpt: We recently reported on a study of 1,070 genes and how they contradicted each other in a couple dozen yeast species. Specifically, evolutionists computed the evolutionary tree, using all 1,070 genes, showing how the different yeast species are related. This tree that uses all 1,070 genes is called the concatenation tree. They then repeated the computation 1,070 times, for each gene taken individually. Not only did none of the 1,070 trees match the concatenation tree, they also failed to show even a single match between themselves. In other words, out of the 1,071 trees, there were zero matches. Yet one of the fundamental predictions of evolution is that different features should generally agree. It was “a bit shocking” for evolutionists, as one explained: “We are trying to figure out the phylogenetic relationships of 1.8 million species and can’t even sort out 20 yeast.” In fact, as the figure above shows, the individual gene trees did not converge toward the concatenation tree. Evolutionary theory does not expect all the trees to be identical, but it does expect them to be consistently similar. They should mostly be identical or close to the concatenation tree, with a few at farther distances from the concatenation tree. Evolutionists have clearly and consistently claimed this consilience as an essential prediction. But instead, on a normalized scale from zero to one (where zero means the trees are identical), the gene trees were mostly around 0.4 from the concatenation tree with a huge gap in between. There were no trees anywhere close to the concatenation tree. This figure is a statistically significant, stark falsification of a highly acclaimed evolutionary prediction. http://darwins-god.blogspot.com/2013/06/here-are-those-incongruent-trees-from.html

Dr, Hunter further comments on the disingenuous nature in which Darwinists tried to 'massage the data' in order to give the preferred answer that fits their theory of common descent.

That Yeast Study is a Good Example of How Evolutionary Theory Works – Cornelius Hunter – June 2013 Excerpt:,,, The evolutionists tried to fix the problem with all kinds of strategies. They removed parts of genes from the analysis, they removed a few genes that might have been outliers, they removed a few of the yeast species, they restricted the analysis to certain genes that agreed on parts of the evolutionary tree, they restricted the analysis to only those genes thought to be slowly evolving, and they tried restricting the gene comparisons to only certain parts of the gene. These various strategies each have their own rationale. That rationale may be dubious, but at least there is some underlying reasoning. Yet none of these strategies worked. In fact they sometimes exacerbated the incongruence problem. What the evolutionists finally had to do, simply put, was to select the subset of the genes or of the problem that gave the right evolutionary answer. They described those genes as having “strong phylogenetic signal.” And how do we know that these genes have strong phylogenetic signal. Because they give the right (preferred) answer. This is an example of a classic tendency in science known as confirmation bias.,,, http://darwins-god.blogspot.com/2013/06/that-yeast-study-is-good-example-of-how.html

Yet, no matter how much Darwinists may 'massage the data' in order to try to get the data to fit their preferred theory, the fact of the matter is that, number one, they have no evidence that the transformation of one species into another species is remotely feasible,

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

Number two, the genetic data, when looked at clearly and soberly without Darwinian blinders on, actually supports Intelligent Design not Darwinian evolution:

New Paper by Winston Ewert Demonstrates Superiority of Design Model - Cornelius Hunter - July 20, 2018 Excerpt: Ewert’s three types of data are: (i) sample computer software, (ii) simulated species data generated from evolutionary/common descent computer algorithms, and (iii) actual, real species data. Ewert’s three models are: (i) a null model which entails no relationships between any species, (ii) an evolutionary/common descent model, and (iii) a dependency graph model. Ewert’s results are a Copernican Revolution moment. First, for the sample computer software data, not surprisingly the null model performed poorly. Computer software is highly organized, and there are relationships between different computer programs, and how they draw from foundational software libraries. But comparing the common descent and dependency graph models, the latter performs far better at modeling the software “species.” In other words, the design and development of computer software is far better described and modeled by a dependency graph than by a common descent tree. Second, for the simulated species data generated with a common descent algorithm, it is not surprising that the common descent model was far superior to the dependency graph. That would be true by definition, and serves to validate Ewert’s approach. Common descent is the best model for the data generated by a common descent process. Third, for the actual, real species data, the dependency graph model is astronomically superior compared to the common descent model. Where It Counts Let me repeat that in case the point did not sink in. Where it counted, common descent failed compared to the dependency graph model. The other data types served as useful checks, but for the data that mattered — the actual, real, biological species data — the results were unambiguous. Ewert amassed a total of nine massive genetic databases. In every single one, without exception, the dependency graph model surpassed common descent. Darwin could never have even dreamt of a test on such a massive scale. Darwin also could never have dreamt of the sheer magnitude of the failure of his theory. Because you see, Ewert’s results do not reveal two competitive models with one model edging out the other. We are not talking about a few decimal points difference. For one of the data sets (HomoloGene), the dependency graph model was superior to common descent by a factor of 10,064. The comparison of the two models yielded a preference for the dependency graph model of greater than ten thousand. Ten thousand is a big number. But it gets worse, much worse. Ewert used Bayesian model selection which compares the probability of the data set given the hypothetical models. In other words, given the model (dependency graph or common descent), what is the probability of this particular data set? Bayesian model selection compares the two models by dividing these two conditional probabilities. The so-called Bayes factor is the quotient yielded by this division. The problem is that the common descent model is so incredibly inferior to the dependency graph model that the Bayes factor cannot be typed out. In other words, the probability of the data set, given the dependency graph model, is so much greater than the probability of the data set given the common descent model, that we cannot type the quotient of their division. Instead, Ewert reports the logarithm of the number. Remember logarithms? Remember how 2 really means 100, 3 means 1,000, and so forth? Unbelievably, the 10,064 value is the logarithm (base value of 2) of the quotient! In other words, the probability of the data on the dependency graph model is so much greater than that given the common descent model, we need logarithms even to type it out. If you tried to type out the plain number, you would have to type a 1 followed by more than 3,000 zeros. That’s the ratio of how probable the data are on these two models! By using a base value of 2 in the logarithm we express the Bayes factor in bits. So the conditional probability for the dependency graph model has a 10,064 advantage over that of common descent. 10,064 bits is far, far from the range in which one might actually consider the lesser model. See, for example, the Bayes factor Wikipedia page, which explains that a Bayes factor of 3.3 bits provides “substantial” evidence for a model, 5.0 bits provides “strong” evidence, and 6.6 bits provides “decisive” evidence. This is ridiculous. 6.6 bits is considered to provide “decisive” evidence, and when the dependency graph model case is compared to comment descent case, we get 10,064 bits. But It Gets Worse The problem with all of this is that the Bayes factor of 10,064 bits for the HomoloGene data set is the very best case for common descent. For the other eight data sets, the Bayes factors range from 40,967 to 515,450. In other words, while 6.6 bits would be considered to provide “decisive” evidence for the dependency graph model, the actual, real, biological data provide Bayes factors of 10,064 on up to 515,450. We have known for a long time that common descent has failed hard. In Ewert’s new paper, we now have detailed, quantitative results demonstrating this. And Ewert provides a new model, with a far superior fit to the data. https://evolutionnews.org/2018/07/new-paper-by-winston-ewert-demonstrates-superiority-of-design-model/

bornagain77

EDTA - the paper that found this is here (and there's a blog post here). From the blogpost:

We know that introns have been lost in yeast because the genes of related species have lots of introns.

In the paper, the authors explain that they mapped 250 introns in 20 yest species, and looked at their patterns of loss and gain (using a standard phylogenetic approach). Bob O'H

Our Cells Are Filled With ‘Junk DNA’ — Here’s Why We Need It Much of our genome has no apparent purpose. Is it so-called “junk DNA” or do we simply not understand it? By Daniel Bastardo Blanco - August 13, 2019 Excerpt: In a study published in Molecular Biology of the Cell in 2008, scientists cleaned junk DNA from yeast’s genome. For particular genes, they got rid of introns — the sections that get chopped away after DNA transcription. They reported the intron removal had no significant consequences for the cells under laboratory conditions, supporting the notion that they don’t have any function. But studies published in Nature this year argued otherwise. When food is scarce, researchers found these sequences are essential for yeast survival. The usefulness of these introns might depend on the context, these studies argue — still a far cry from being junk. https://www.discovermagazine.com/health/our-cells-are-filled-with-junk-dna-heres-why-we-need-it “Junk DNA” Suffers a Blow as Nature Papers Find “Global Function” for Introns in Budding Yeast Evolution News - January 21, 2019 Introns in Budding Yeast Saccharomyces cerevisiae possesses a compact genome, containing only 295 introns which are found across 280 genes (Hooks et al., 2014; Neuvéglise et al., 2011). Most of these introns are shorter than 500 nucleotides in length and only nine yeast genes possess more than one intron (Neuvéglise et al., 2011; Spingola et al., 1999). The latest issue of Nature carries a paper on the functions of introns in budding yeast (Parenteau et al., 2019). Here is the Abstract: Introns are ubiquitous features of all eukaryotic cells. Introns need to be removed from nascent messenger RNA through the process of splicing to produce functional proteins. Here we show that the physical presence of introns in the genome promotes cell survival under starvation conditions. A systematic deletion set of all known introns in budding yeast genes indicates that, in most cases, cells with an intron deletion are impaired when nutrients are depleted. This effect of introns on growth is not linked to the expression of the host gene, and was reproduced even when translation of the host mRNA was blocked. Transcriptomic and genetic analyses indicate that introns promote resistance to starvation by enhancing the repression of ribosomal protein genes that are downstream of the nutrient-sensing TORC1 and PKA pathways. Our results reveal functions of introns that may help to explain their evolutionary preservation in genes, and uncover regulatory mechanisms of cell adaptations to starvation. [Emphasis added.] The paper further explains: In this study, we present what is — to our knowledge — the first complete collection of yeast strains each with a deletion of a specific intron. The analyses of this collection provide direct evidence for global functions of introns that may explain their preservation during evolution, regardless of the function or expression of the host gene of the intron. A Library of Yeast Strains The researchers, led by Sherif Abou Elela of the University of Sherbrooke, systematically constructed a library of yeast strains, deleting a different intron from each of the 295 strains. The result of deleting introns was a stunting of the cell growth in nutrient-depleted environments, even though there was not much impact on the cells whose environment was not depleted of nutrients. Elela and his team determined that approximately 90 percent of introns across the genome of Saccharomyces had this result when removed. In their own words, “We conclude that introns are specifically required for growth in the stationary phase of the culture when nutrients are depleted.” In their discussion, they note: We have shown that introns affect cell growth in response to nutrient depletion, regardless of host-gene function. Deleting a single intron reduces the capacity of cells to withstand nutrient depletion or starvation (Figs. 1, 2). Notably, introns could independently rescue the defects caused by intron deletion, even when their host protein was not produced (Fig. 3). Transcriptome analyses indicate that introns promote resistance to nutrient depletion by inhibiting a common set of genes that are associated with translation and respiration (Fig. 5). These intron effects appear to couple the TOR and PKA pathways to the repression of ribosome biogenesis, on the basis of nutrient concentration (Fig. 6 and Extended Data Fig. 10b, c). Together, the data present a paradigm of intron function in which the presence of introns directly contributes to cell growth in a way that is independent of the function of their host gene. https://evolutionnews.org/2019/01/junk-dna-suffers-a-blow-as-nature-papers-find-global-function-for-introns-in-budding-yeast/ Introns are not “junk DNA” - 2016 Excerpt: Introns, originally called “junk DNA“, are not present in the mature RNA and do not influence the final protein product. So why do cells waste energy, copying introns just to remove them immediately afterwards? Returning to the music analogy, imagine itunes gives in to complaints and removes the white noise. Customers are surprised to find that suddenly some songs are not downloading as efficiently. Some can only be downloaded a few times per day, others will not download at all, and the most popular songs are hit the hardest That’s what happens when scientists try to express genes without introns. For many genes, the intronless version does not yield as many copies of RNA. Further, some genes are completely dependent on this “intron-mediated enhancement” or “IME”. Only certain introns exhibit IME, and they tend to be found in the most fundamental genes, those that are expressed all the time. IME can increase the expression of genes anywhere from 2 to 20 fold in plants, animals, and fungi. In my lab, we study IME in plants, because introns are routinely used to increase expression of genes in crops from herbicide-tolerant soybeans to nutritionally enhanced rice. Better understanding IME could enable us to design synthetic introns that maximize gene expression potential. https://escapingthebench.com/2016/04/03/introns-versus-junk-dna/ Matheson’s Intron Fairy Tale - Richard Sternberg - June 3, 2010 Excerpt: The failure to recognize the importance of introns “may well go down as one of the biggest mistakes in the history of molecular biology.” -John Mattick, Molecular biologist, University of Queensland, quoted in Scientific American https://evolutionnews.org/2010/06/mathesons_intron_fairy_tale/ The Fact-Free “Science” of Matheson, Hunt and Moran: Ridicule Instead of Reason, Authority Instead of Evidence - Jonathan Wells - June 8, 2010 Excerpt: In his June 3 blog post, Sternberg cited a 2010 Nature article that begins, “Transcripts from approximately 95% of multi-exon human genes are spliced in more than one way.” (Exons are the protein-coding parts of genes.) Sternberg calculated that a reasonable estimate for the number of human introns that undergo alternative splicing was thus 0.9 x 190,000 = 171,000. The same Nature article reports that “in most cases the resulting transcripts are variably expressed between different cell and tissue types,” suggesting that many alternatively spliced introns serve important biological functions. Sternberg concluded that even if his estimate were off by a factor of two, the number of functional introns would still be far greater than Matheson’s 1,000. https://evolutionnews.org/2010/06/the_factfree_science_of_mathes/ Shoddy Engineering or Intelligent Design? Case of the Mouse’s Eye Richard Sternberg - April 29, 2009 Excerpt: Reporting in the journal Cell, Irina Solovei and coworkers have just discovered that, in contrast to the nucleus organization seen in ganglion and bipolar cells of the retina, a remarkable inversion of chromosome band localities occurs in the rod photoreceptors of mammals with night vision (Solovei I, Kreysing M, Lanctôt C, Kösem S, Peichl L, Cremer T, Guck J, Joffe B. 2009. “Nuclear Architecture of Rod Photoreceptor Cells Adapts to Vision in Mammalian Evolution.” Cell 137(2): 356-368). First, the C-bands of all the chromosomes including the centromere coalesce in the center of the nucleus to produce a dense chromocenter. Keep in mind that the DNA backbone of this chromocenter in different mammals is repetitive and highly species-specific. Second, a shell of LINE-rich G-band sequences surrounds the C-bands. Finally, the R-bands including all examined protein-coding genes are placed next to the nuclear envelope. The nucleus of this cell type is also smaller so as to make the pattern more compact. This ordered movement of billions of basepairs according to their “barcode status” begins in the rod photoreceptor cells at birth, at least in the mouse, and continues for weeks and months. Why the elaborate repositioning of so much “junk” DNA in the rod cells of nocturnal mammals? The answer is optics. A central cluster of chromocenters surrounded by a layer of LINE-dense heterochromatin enables the nucleus to be a converging lens for photons, so that the latter can pass without hindrance to the rod outer segments that sense light. In other words, the genome regions with the highest refractive index — undoubtedly enhanced by the proteins bound to the repetitive DNA — are concentrated in the interior, followed by the sequences with the next highest level of refractivity, to prevent against the scattering of light. The 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 — that the data only point to the lack of design and suboptimality — remind them of the rod cell nuclei of the humble mouse. https://evolutionnews.org/2009/04/shoddy_engineering_or_intellig/

bornagain77

Question about this point, Sev: >"About 98% of the introns in modern yeast (Saccharomyces cerevisiae) have been eliminated during evolution form a common ancestor that probably had about 18,000 introns..." Since all we have to work with are the modern forms of yeast, how do they know there used to be more introns which are now gone? EDTA

4. Researchers routinely construct intronless versions of eukaryotic genes and they function normally when re-inserted into the genome. You can live without one of your two kidneys, without your tonsils or your spleen. And even without your two legs. That does not mean they are 'functionless'. Truthfreedom

'We do not know the meaning of 'function'. But we know for sure that when that meaning embarrasses us, then it is not the good one'. Truthfreedom

'@5 Fasteddious: 'This is sort of like the “we don’t use 90% of our brain” myth that was common a few decades ago. I did not see many people sign up for voluntary lobotomy.' Oh, that silly one :) I had thougth science and myth were opposites. Truthfreedom

OK Sev, why don't you put your genome where your mouth is: how much of your DNA do you want to get rid of as "junk"? Just think, if 90, or 50 or even 20% of your genome is really useless junk, then you don't need it. Your cells would be more efficient without all that junk, right? Just think, you'd be a superman without having to carry around that excess baggage! So go ahead, which parts do you want to toss out? In a few years you'll be able to find a clinic willing to delete "bad" genes, so why not remove all the "junk" you have identified. No takers? Oh, maybe you'll hang onto all that DNA? After all, if the functional parts have gone from 2% to 10% to 30% or even 80%, who knows, maybe science will find out 98% of it is needed by some cell or other at some point in your development. This is sort of like the "we don't use 90% of our brain" myth that was common a few decades ago. I did not see many people sign up for voluntary lobotomy. Fasteddious

The Function Wars: Part I. Quibbling about the meaning of the word "function"

The ENCODE Consortium tried to redefine the word “function” to include any biological activity that they could detect using their genome-wide assays. This was not helpful since it included a huge number of sites and sequences that result from spurious (nonfunctional) binding of transcription factors or accidental transcription of random DNA sequences to make junk RNA [see What did the ENCODE Consortium say in 2012?].. I believe that this strange way of redefining biological function was a deliberate attempt to discredit junk DNA. It was quite successful since much of the popular press interpreted the ENCODE results as refuting or disproving junk DNA. I believe that the leaders of the ENCODE Consortium knew what they were doing when they decided to hype their results by announcing that 80% of the human genome is functional [see The Story of You: Encode and the human genome – video, Science Writes Eulogy for Junk DNA]..

The Many Meanings of “Function” The issue of whether a large part of our genome is junk is not just a philosophical debate about the meaning of “function” but a large part of the Germain et al. paper is devoted to just that. The authors discuss two philosophical definitions called the causal role account of function and the selected-effect account. I find their discussion tedious and almost incomprehensible. The distinction between the two definitions is explained much better in Doolittle (2013) and Doolittle et al. (2014) but both discussions suffer from the over-emphasis of a false premise; namely, that it’s possible to define “function” in an unambiguous way that sheds light on the junk DNA debate. The paper by Graur et al. (2013) suffers from the same problem. Those authors come down firmly on the side of selected-effect functions although they recognize that, “Estimates of functionality based on conservation are likely to be, well, conservative.” The best way to define function, according to Graur et al. is in terms of whether losing it has consequences. This is the best working definition, in my opinion: a sequence is functional if deleting it from the genome has an effect on the survivability of the organism or its progeny. This is the definition I’ve been using for almost two decades [see Junk DNA Poll].

Seversky

Are introns mostly junk?

There are many reasons for thinking that introns are mostly junk DNA. 1. The size and sequence of introns in related species are not conserved and almost all of the sequences are evolving at the rate expected for neutral substitutions and fixation by drift. 2. Many species have lost introns or reduced their lengths drastically suggesting that the presence of large introns can be detrimental in some cases (probably large populations). 3. After decades of searching, there are very few cases where introns and/or parts of introns have been shown to be essential. 4. Researchers routinely construct intronless versions of eukaryotic genes and they function normally when re-inserted into the genome. 5. Intron sequences are often littered with transposon and viral sequences that have inserted into the intron and this is not consistent with the idea that intron sequences are important. 6. About 98% of the introns in modern yeast (Saccharomyces cerevisiae) have been eliminated during evolution form a common ancestor that probably had about 18,000 introns [Yeast loses its introns]. This suggests that there was no selective pressure to retain those introns over the past 100 million years. 7. About 245/295 of the remaining introns in yeast have been artificially removed by researchers who are constructing an artificial yeast genome suggesting that over 80% of the introns that survived evolutionary loss are also junk [Yeast loses its introns].

Seversky

'When function is found for Junk DNA then it is evidence that God does exist, right?'. Hehehe. Atheist theologians will find a way during their next conclave to solve the dilemma. 'It is 'junk'. 'Oh wait, it is functional!' 'We guessed it!' 'Oh wait, but not 'functional-functional'. 'Functional as we see fit!' 'Did we say 'junk'? 'Oh my dawkins, ain't Science (with caps, unlike 'god') cool'? Insert philosophical add-on (e.g): 'God does not exist! We know it, although our brains are kluge! Evolved brains are un-reliable except when related to atheistic Evolution (with caps, unlike 'god'!). Then you can trust them! No doubts! And no faith required here! You do not even need to think about the details! It is true and it will be forever and ever. For sæcula sæculorum.' Amen. Truthfreedom

Dawkins illustrated the importance of this issue (at least for people like him):

“creationists might spend some earnest time speculating on why the Creator should bother to litter genomes with untranslated pseudogenes and junk tandem repeat DNA.” ("The Information Challenge," (1998) The Skeptic, Pg.18)

It's not much of an argument: Junk DNA is non-functional. Therefore, God does not exist. When function is found for Junk DNA then it is evidence that God does exist, right? Silver Asiatic