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Anyone else for the myth of junk DNA? Richard Dawkins, for one

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The Selfish Gene

He certainly drew the desired Darwinian conclusion:

“The amount of DNA in organisms,” Dawkins wrote in 1976, “is more than is strictly necessary for building them: A large fraction of the DNA is never translated into protein. From the point of view of the individual organism this seems paradoxical. If the ‘purpose’ of DNA is to supervise the building of bodies, it is surprising to find a large quantity of DNA which does no such thing. Biologists are racking their brains trying to think what useful task this apparently surplus DNA is doing. But from the point of view of the selfish genes themselves, there is no paradox. The true ‘purpose’ of DNA is to survive, no more and no less. The simplest way to explain the surplus DNA is to suppose that it is a parasite, or at best a harmless but useless passenger, hitching a ride in the survival machines created by the other DNA. “

Jonathan Wells, author of The Myth of Junk DNA, p. 20

And he was wrong as a result. Just like these folk:

Jerry Coyne and Michael Shermer. Oh, and Francis Collins, though he may be coming round.

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Comments
ba77: I listened to the podcasts and looked over the website, but couldn’t find anything regarding this topic. But about the “failed prediction”. Are you saying that given a) that junk dna is real and b) selective pressure to shrink the genome, that the genome shouldn’t shrink? What do you think the prediction should be given those premises? That the genome should grow? Stay the same size?goodusername
July 18, 2011
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a more recent podcast: Failed Predictions of Evolutionists - Cornelius Hunter - audio http://intelligentdesign.podomatic.com/player/web/2009-11-09T15_20_49-08_00bornagain77
July 18, 2011
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goodusername you ask: 'Isn’t this exactly what we’d expect if much of the genome is junk dna?' Actually no, but failed predictions never stopped neo-Darwinists before so I don't it will bother you now. Darwin’s Predictions http://www.darwinspredictions.com/ Darwin's Predictions With Cornelius Hunter - podcast with Cornelius Hunter http://intelligentdesign.podomatic.com/entry/eg/2009-11-04T16_03_23-08_00bornagain77
July 18, 2011
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“There is strong positive correlation, however, between the amount of DNA and the volume of a cell and its nucleus – which effects the rate of cell growth and division. Furthermore, in mammals there is a negative correlation between genome size and rate of metabolism. Bats have very high metabolic rates and relatively small genomes. In birds, there is a negative correlation between C-value and resting metabolic rate. In salamanders, there is also a negative correlation between genome size and the rate of limb regeneration. Jonathan Wells – The Myth Of Junk DNA – page 85” --I’ve seen this quoted a number of times, apparently as an argument against junk dna, although I’m not sure why. Isn’t this exactly what we’d expect if much of the genome is junk dna? If there is selective pressure to increase metabolism, consequently there is selective pressure to decrease cell size, and consequently selective pressure to decrease the genome size. If the genomes of animals with higher metabolism didn’t shrink, despite the selective pressure to do so, than presumably that would mean there isn’t much room for their genomes to shrink, which would hardly square with the idea that much of the genome is junk.goodusername
July 18, 2011
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Mung: 1. DNA does more than build an organism - it also ensures it functions 2. Not all DNA codes for proteins 3. Some DNA is junk, i.e. does nothing, including pseudogenes, ervs and huge repeats 4. Onions appear to have a large amount of junk 5. Evolutionary theory suggests that unless there is an organismal cost to making DNA, junk will tend to accumulate. 6. The existence of junk DNA is consistent with Darwinian evolution 7. It is possibly consistent with ID too. What is your point?Elizabeth Liddle
July 18, 2011
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Time for review:
Dawkins is right. Many very similar species have very different genome sizes.
Therefore, ID must be false.Mung
July 17, 2011
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Time for review:
Dawkins is right. Many very similar species have very different genome sizes. For example, onions. Many “simpler” species, like lungfish and ferns, have genomes up to 100 times bigger than the human genome. Thus, it really is true that many species have way more DNA than is needed to build them.
Oh my. Therefore, ID must be false.Mung
July 17, 2011
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Nick Matzke:
Mung can’t claim it’s a strawman to say that ID expects “junk DNA” to have informational function.
That would be just stupid. By definition junk DNA has no function. But that's not what I was claiming, so it's a red herring. So Nick. Straw man. Red herring. So typical of "arguments" against ID.Mung
July 17, 2011
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LOL, Elizabeth Liddle vs. Nick Matzke.
I have no idea, Mung. It’s patently untrue. A lot of DNA is for ensuring that an organism actually functions.
Yes Nick, it's patently untrue. That means it's obviously untrue. One hardly needs an argument to see so. Yet that doesn't stop you. And perhaps at least a teeny bit of DNA is there for the purpose of reproduction. And I think it's also funny how the silly claim relied on purpose. Come back when you've left the strawman at home Nick. Others may fall for it, I won't.Mung
July 17, 2011
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Dembski 1998: "If, on the other hand, organisms are designed, we expect DNA, as much as possible, to exhibit function...Design encourages scientists to look for function where evolution discourages it." Nick: ...“Mung can’t claim it’s a strawman to say that ID expects “junk DNA” to have informational function." Wiggle it in there baby.junkdnaforlife
July 16, 2011
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LOL, Mung vs. other pro-ID commentators: Mung:
Straw-man, Straw-man. Nick, do you seriously want us to believe that the sole purpose of all onion DNA is to build an onion and that the sole purpose all of human DNA is to build a human? Why would we believe such a thing?
If, on the other hand, organisms are designed, we expect DNA, as much as possible, to exhibit function. And indeed, the most recent findings suggest that designating DNA as “junk” merely cloaks our current lack of knowledge about function. Design encourages scientists to look for function where evolution discourages it.”
And Nick exactly how does finding multiple layers of overlapping functional complexity, in the genome, help your neo-Darwinian case in the least??? Would not finding complexity stacked on top of complexity provide exponentially larger levels of constraint on neo-Darwinism???
If the latter arguments are made, then Mung can't claim it's a strawman to say that ID expects "junk DNA" to have informational function.NickMatzke_UD
July 16, 2011
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Nick, I remember a few years back when many neo-Darwinists denied that information was even in DNA!!! ,,,But then again it never was about science in the first place was it Nick???,, Especially since you cannot even justify doing science within your neo-Darwinian worldview!!!!,,, as clearly noted here: https://uncommondescent.com/darwinism/anyone-else-for-the-myth-of-junk-dna-richard-dawkins-for-one/#comment-390161 And Nick exactly how does finding multiple layers of overlapping functional complexity, in the genome, help your neo-Darwinian case in the least??? Would not finding complexity stacked on top of complexity provide exponentially larger levels of constraint on neo-Darwinism??? Poly-Functional Complexity equals Poly-Constrained Complexity http://docs.google.com/Doc?docid=0AYmaSrBPNEmGZGM4ejY3d3pfMjdoZmd2emZncQ "There is abundant evidence that most DNA sequences are poly-functional, and therefore are poly-constrained. This fact has been extensively demonstrated by Trifonov (1989). For example, most human coding sequences encode for two different RNAs, read in opposite directions i.e. Both DNA strands are transcribed ( Yelin et al., 2003). Some sequences encode for different proteins depending on where translation is initiated and where the reading frame begins (i.e. read-through proteins). Some sequences encode for different proteins based upon alternate mRNA splicing. Some sequences serve simultaneously for protein-encoding and also serve as internal transcriptional promoters. Some sequences encode for both a protein coding, and a protein-binding region. Alu elements and origins-of-replication can be found within functional promoters and within exons. Basically all DNA sequences are constrained by isochore requirements (regional GC content), “word” content (species-specific profiles of di-, tri-, and tetra-nucleotide frequencies), and nucleosome binding sites (i.e. All DNA must condense). Selective condensation is clearly implicated in gene regulation, and selective nucleosome binding is controlled by specific DNA sequence patterns - which must permeate the entire genome. Lastly, probably all sequences do what they do, even as they also affect general spacing and DNA-folding/architecture - which is clearly sequence dependent. To explain the incredible amount of information which must somehow be packed into the genome (given that extreme complexity of life), we really have to assume that there are even higher levels of organization and information encrypted within the genome. For example, there is another whole level of organization at the epigenetic level (Gibbs 2003). There also appears to be extensive sequence dependent three-dimensional organization within chromosomes and the whole nucleus (Manuelides, 1990; Gardiner, 1995; Flam, 1994). Trifonov (1989), has shown that probably all DNA sequences in the genome encrypt multiple “codes” (up to 12 codes). Dr. John Sanford; Genetic Entropy 2005 notes as to higher level functionality: On Not Reading Signature in the Cell: A Response to Francisco Ayala Excerpt: In general, SINEs (and thus Alus) allow genetic information to be retrieved in multiple different ways from the same DNA data files depending on the specific needs of different cell types or tissues (in different species-specific contexts). In particular, Alu sequences perform many taxon-specific lower-level genomic formatting functions such as: (1) providing alternative start sites for promoter modules in gene expression–somewhat like sectoring on a hard drive (Faulkner et al., 2009; Faulkner and Carninci, 2009); (2) suppressing or “silencing” RNA transcription (Trujillo et al., 2006); (3) dynamically partitioning one gene file from another on the chromosome (Lunyak et al., 2007); (4) providing DNA nodes for signal transduction pathways or binding sites for hormone receptors (Jacobsen et al., 2009; Laperriere et al., 2004); (5) encoding RNAs that modulate transcription (Allen et al., 2004; Espinoza et al., 2004; Walters et al., 2009); and (6) encoding or regulating microRNAs (Gu et al., 2009; Lehnert et al., 2009). In addition to these lower-level genomic formatting functions, SINEs (including Alus) also perform species-specific higher-level genomic formatting functions such as: (1) modulating the chromatin of classes of GC-rich housekeeping and signal transduction genes (Grover et al., 2003, 2004; Oei et al., 2004; see also Eller et al., 2007); (2) “bar coding” particular segments for chromatin looping between promoter and enhancer elements (Ford and Thanos, 2010); (3) augmenting recombination in sequences where Alus occur (Witherspoon et al., 2009); and (4) assisting in the formation of three-dimensional chromosome territories or “compartments” in the nucleus (Kaplan et al., 1993; see also Pai and Engelke, 2010). Moreover, Alu sequences also specify many species-specific RNA codes. In particular, they provide: (1) signals for alternative RNA splicing (i.e., they generate multiple messenger RNAs from the same type of precursor transcript) (Gal-Mark et al., 2008; Lei and Vorechovsky, 2005; Lev-Maor et al., 2008) and (2) alternative open-reading frames (exons) (Lev-Maor et al., 2007; Lin et al., 2008; Schwartz et al., 2009). Alu sequences also (3) specify the retention of select RNAs in the nucleus to silence expression (Chen et al., 2008; Walters et al., 2009); (4) regulate the RNA polymerase II machinery during transcription (Mariner et al., 2008; Yakovchuk et al., 2009; Walters et al., 2009); and (5) provide sites for Adenine-to-Inosine RNA editing, a function that is essential for both human development and species-specific brain development (Walters et al., 2009). Contrary to Ayala’s claim, Alu sequences (and other mammalian SINEs) are not distributed randomly but instead manifest a similar “bar-code” distribution pattern along their chromosomes (Chen and Manuelidis, 1989; Gibbs et al., 2004; Korenberg and Rykowski, 1988). Rather like the distribution of the backslashes, semi-colons and spaces involved in the formatting of software code, the “bar-code” distribution of Alu sequences (and other SINEs) reflects a clear functional logic, not sloppy editing or random mutational insertions. For example, Alu sequences are preferentially located in and around protein-coding genes as befits their role in regulating gene expression (Tsirigos and Rigoutsos, 2009). They occur mainly in promoter regions–the start sites for RNA production–and in introns, the segments that break up the protein-coding stretches. Outside of these areas, the numbers of Alu sequences sharply decline. Further, we now know that Alu sequences are directed to (or spliced into) certain preferential hotspots in the genome by the protein complexes or the “integrative machinery” of the cell’s information processing system (Levy et al., 2010). This directed distribution of Alu sequences enhances the semantic and syntactical organization of human DNA. It appears to have little to do with the occurrence of random insertional mutations, contrary to the implication of Ayala’s “sloppy editor” illustration and argument. (page down for 33 references of ALU functionality) http://www.stephencmeyer.org/news/2010/03/_this_is_part_2.html And let's not forget Nick,,, Modern Synthesis of Neo-Darwinism Is Dead - Paul Nelson - video http://www.metacafe.com/watch/5548184/ Human Genome “Infinitely More Complex” Than Expected - April 2010 Excerpt: Hayden acknowledged that the “junk DNA” paradigm has been blown to smithereens. “Just one decade of post-genome biology has exploded that view,” she said,,,, Network theory is now a new paradigm that has replaced the one-way linear diagram of gene to RNA to protein. That used to be called the “Central Dogma” of genetics. Now, everything is seen to be dynamic, with promoters and blockers and interactomes, feedback loops, feed-forward processes, and “bafflingly complex signal-transduction pathways.” http://www.creationsafaris.com/crev201004.htm#20100405a Contrary to Darwinian expectations for 'simplicity' at the basis of life, the complexity being uncovered in genomes keeps increasing dramatically as our resolution increases: Most Detailed Annotation of Fruit-Fly Genome Points Way to Understanding All Organisms’ Genomes – December 2010 Excerpt: “We also found an order-of-magnitude increase in the ways that genes are spliced and edited to produce alternate forms of known proteins, thus significantly increasing the complexity of the proteome.”,,, Despite the scrutiny to which the Drosophila genome has been subjected, the researchers found new or altered exons or splice forms in almost three-quarters of Drosophila’s previously annotated genes,,, http://www.sciencedaily.com/releases/2010/12/101222131131.htm Astonishing DNA complexity update Excerpt: The untranslated regions (now called UTRs, rather than ‘junk’) are far more important than the translated regions (the genes), as measured by the number of DNA bases appearing in RNA transcripts. Genic regions are transcribed on average in five different overlapping and interleaved ways, while UTRs are transcribed on average in seven different overlapping and interleaved ways. Since there are about 33 times as many bases in UTRs than in genic regions, that makes the ‘junk’ about 50 times more active than the genes. http://creation.com/astonishing-dna-complexity-update etc.. etc.. etc...bornagain77
July 16, 2011
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Mung:
Straw-man, Straw-man. Nick, do you seriously want us to believe that the sole purpose of all onion DNA is to build an onion and that the sole purpose all of human DNA is to build a human? Why would we believe such a thing?
I have no idea, Mung. It's patently untrue. A lot of DNA is for ensuring that an organism actually functions. Our brains wouldn't work, and we'd be unable to remember anything unless genes in neurons were being expressed to modify neural connections. But I'm not aware that onions do a lot of remembering.Elizabeth Liddle
July 16, 2011
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Mung @ 47: Can you re-read, please, the post of mine you half quoted? Here it is:
Can you find me a citation in which somebody representing “ET” makes the claim that ET predicts that the vast part of DNA in all species will be junk? I would be intrigued to see the reasoning behind such a bizarre claim.
Also please link to where I apparently "insist... that “junk DNA” is a prediction of evolutionary theory." Thanks.Elizabeth Liddle
July 16, 2011
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Mims/Dembski: "As far back as 1994, pro-ID scientist and Discovery Institute fellow Forrest Mims had warned in a letter to Science against assuming that 'junk' DNA was 'useless.'" Science wouldn't print Mims' letter, but soon thereafter, in 1998, leading ID theorist William Dembski repeated this sentiment in First Things: "[Intelligent] design is not a science stopper. Indeed, design can foster inquiry where traditional evolutionary approaches obstruct it. Consider the term "junk DNA." Implicit in this term is the view that because the genome of an organism has been cobbled together through a long, undirected evolutionary process, the genome is a patchwork of which only limited portions are essential to the organism. Thus on an evolutionary view we expect a lot of useless DNA. If, on the other hand, organisms are designed, we expect DNA, as much as possible, to exhibit function. And indeed, the most recent findings suggest that designating DNA as "junk" merely cloaks our current lack of knowledge about function. Design encourages scientists to look for function where evolution discourages it." Nick: At best it has a function in bulk, i.e. the “function” is taking up space, where the actual sequence doesn’t matter as long as it doesn’t cause problems. “There is strong positive correlation, however, between the amount of DNA and the volume of a cell and its nucleus – which effects the rate of cell growth and division. Furthermore, in mammals there is a negative correlation between genome size and rate of metabolism. Bats have very high metabolic rates and relatively small genomes. In birds, there is a negative correlation between C-value and resting metabolic rate. In salamanders, there is also a negative correlation between genome size and the rate of limb regeneration.” Jonathan Wells – The Myth Of Junk DNA – page 85junkdnaforlife
July 16, 2011
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Oops, hit send too soon. Trying again:
Nick, do you seriously want us to believe that the sole purpose of all onion DNA is to build an onion and that the sole purpose all of human DNA is to build a human? Why would we believe such a thing?
Oh really? IDists have proposed a different purpose for DNA? The ID focus, ever since they started talking about junk DNA has been *entirely* on the premise that "junk DNA" is "chock-full" of information that codes for stuff -- gene regulation mostly, which is allegedly necessary for building and maintaining an organism. Based on the table of contents of Wells's book, Wells might have finally realized the problem that wild genome size variation poses for standard ID claims about junk DNA, and tried to paper it over, probably by acknowledging the genome-size vs. cell size correlation, which "Darwinists" have been talking about for decades and which I already addressed. But apart from that? I've read pretty much all of the ID literature and blogs etc. I bet you can't find a single instance of an IDist proposing some function for junk DNA other than hidden coding information for building and maintaining and organism.NickMatzke_UD
July 16, 2011
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Nick, do you seriously want us to believe that the sole purpose of all onion DNA is to build an onion and that the sole purpose all of human DNA is to build a human? Why would we believe such a thing?/
Oh really? IDists have proposed a different purpose for DNA? What is it, pray tell?
NickMatzke_UD
July 16, 2011
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Nick Matzke:
We know where those huge variations in genome size came from: replication of repetitive elements, genome duplications, deletion events, etc.
Well, we think that might be where they come from. But why would events like that occur more often in an onion than in a human? Is this true of all onions? Is this something that seems to happen more often in plants than in animals? You're not comparing onions and humans again are you?Mung
July 15, 2011
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Elizabeth Liddle:
I would be intrigued to see the reasoning behind such a bizarre claim. Says the lady who insists that "junk DNA" is a prediction of evolutionary theory.
Mung
July 15, 2011
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Nick Matzke:
Re: c-value enigma. Ah! Brilliant! That’s exactly what I was talking about (and have been for years).
Hi nick, Certainly you understand that the c-value enigma didn't arise because of intelligent design? I mean, it's an enigma for you. Why should it be an enigma for ID theory? Oh, can i, can i? Puleeeeeze!!! IT'S NOT.Mung
July 15, 2011
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Nick Matzke:
So: why do some onions take *7 human genomes worth of DNA* **more** to build an onion that is basically similar to another onion?
Straw-man, Straw-man. Nick, do you seriously want us to believe that the sole purpose of all onion DNA is to build an onion and that the sole purpose all of human DNA is to build a human? Why would we believe such a thing?Mung
July 15, 2011
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Nick, do you know what a strawman is? Silly me. Of course you do! That's why you're doing it. DOH!Mung
July 15, 2011
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Nick Matzke:
Some onions have 20 human genomes worth of DNA that appears to be completely unnecessary for building an onion.
Strawman. Repeating it more than once and saying 'onion' instead of 'human' doesn't make it not a strawman. ok, so back to basics. Nick, do you know what a strawman is?Mung
July 15, 2011
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Nick claims; 'We know where those huge variations in genome size came from: replication of repetitive elements, genome duplications, deletion events, etc.' And yet real world data states: Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution "Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell--both ones we've discovered so far and ones we haven't--at best extremely limited benefit, since no such process was able to do much of anything. It's critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing--neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered--was of much use." http://www.evolutionnews.org/2009/05/swine_flu_viruses_and_the_edge.html Experimental evolution, loss-of-function mutations, and “the first rule of adaptive evolution” - Michael J. Behe - December 2010 Excerpt: In this paper, I review molecular changes underlying some adaptations, with a particular emphasis on evolutionary experiments with microbes conducted over the past four decades. I show that by far the most common adaptive changes seen in those examples are due to the loss or modification of a pre-existing molecular function, and I discuss the possible reasons for the prominence of such mutations. http://www.journals.uchicago.edu/doi/abs/10.1086/656902 Again I would like to emphasize, I’m not arguing Darwinism cannot make complex functional systems, the data on malaria, and the other examples, are a observation that it does not. In science observation beats theory all the time. So Professor (Richard) Dawkins can speculate about what he thinks Darwinian processes could do, but in nature Darwinian processes have not been shown to do anything in particular. Michael Behe - 46 minute mark of video lecture on 'The Edge of Evolution' for C-SPAN https://uncommondescent.com/intelligent-design/michael-behe-lecture-recommend/comment-page-1/#comment-361037 Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) - October 2010 Excerpt: "Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, "This research really upends the dominant paradigm about how species evolve," said ecology and evolutionary biology professor Anthony Long, the primary investigator. http://www.arn.org/blogs/index.php/literature/2010/10/07/experimental_evolution_in_fruit_flies Epistasis between Beneficial Mutations - July 2011 Excerpt: We found that epistatic interactions between beneficial mutations were all antagonistic—the effects of the double mutations were less than the sums of the effects of their component single mutations. We found a number of cases of decompensatory interactions, an extreme form of antagonistic epistasis in which the second mutation is actually deleterious in the presence of the first. In the vast majority of cases, recombination uniting two beneficial mutations into the same genome would not be favored by selection, as the recombinant could not outcompete its constituent single mutations. https://uncommondescent.com/epigenetics/darwins-beneficial-mutations-do-not-benefit-each-other/ further note as to functionality of 'junk' DNA: Gene Regulatory Networks in Embryos Depend on Pre-existing Spatial Coordinates - jonathan Wells - July 2011 Excerpt: The development of metazoan embryos requires the precise spatial deployment of specific cellular functions. This deployment depends on gene regulatory networks (GRNs), which operate downstream of initial spatial inputs (E. H. Davidson, Nature 468 [2010]: 911). Those initial inputs depend, in turn, on pre-existing spatial coordinate systems. In Drosophila oocytes, for example, spatial localization of the earliest-acting elements of the maternal GRN depends on the prior establishment of an anteroposterior body axis by antecedent asymmetries in the ovary. Those asymmetries appear to depend on cytoskeletal and membrane patterns rather than on DNA sequences,,, http://www.evolutionnews.org/2011/07/paul_nelson_jonathan_wells_tak048301.html etc.. etc.. etc.. So Nick, what am I to believe the actual evidence or what you dogmatically want the evidence to say so as to conform to your atheistic worldview????bornagain77
July 15, 2011
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"You do not know for a fact that it is unnecessary. What works for an onion will not necessarily work for a penguin, a head of cabbage, or a human being." True. But we see similar wide variations in genome size in many, many groups. "You do not know for a fact that it is unnecessary." True, we don't know it for a fact. But a lot of very basic, very simple data points that way. Yet for some reason the IDists are trumpetting from the hilltops the idea that junk DNA is pure myth, that evolutionists were dumb to believe it, etc., etc., when in fact the actual data and actual science still say a huge amount of DNA lacks any very sexy informational "function." "This is another unwarranted assertion." This is far, far more true about the ID side's statements on the junk DNA issue. "Also, there still is no evolutionary explanation of where the DNA came from in the first place." We know where those huge variations in genome size came from: replication of repetitive elements, genome duplications, deletion events, etc. The origin of life itself? Different topic entirely, start a new thread for that.NickMatzke_UD
July 15, 2011
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Arthur : Thank you for the links; they made for some deep but interesting reading. I did note, however, that as much as the blogger touted the fact that this discovery didn't reflect favorably on ID, he did write that, "the supposed functional swaths of non-coding junk DNA may be nothing more than parts of the genome that encode, and lead to the production of, “junk” RNA (if I may so bold as to coin a phrase)." Notice the word "may". In other words, it's not entirely supportive of Darwinian evolution, either, simply because we don't have all the answers right now. Also, the first linked essay noted that there might be some "hitherto hitherto overlooked aspects of promoter and chromatin structure and function." In other words, it might not all be junk piling on top of junk; that's an unwarranted assertion. Nick writes, "...because an awful lot of the DNA in many genomes looks like, basically, junk. It’s unnecessary. We know this because nearly identical organisms don’t have it and are just fine." You do not know for a fact that it is unnecessary. What works for an onion will not necessarily work for a penguin, a head of cabbage, or a human being. This is another unwarranted assertion. Also, there still is no evolutionary explanation of where the DNA came from in the first place.Barb
July 15, 2011
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Jonin:
We’re addressing ET false predictions (and ET bishop’s false claims too) about the ***vast part*** of junk DNA in all species, not some strings of *apparent* “junk” value that seem to exist in DNA.
Can you find me a citation in which somebody representing "ET" makes the claim that ET predicts that the vast part of DNA in all species will be junk? I would be intrigued to see the reasoning behind such a bizarre claim.Elizabeth Liddle
July 15, 2011
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Tell you what Nick, since you think you can design a genome better than the one we find in life, lay it all out for me. I am a willing listener. But something tells me you are not going to be embarrassing God anytime soon!!!
*You ID guys* are the ones saying that the genome is like computer code, it's information-dense, and it's mostly functional, and that scientists were stupid for thinking that a lot of it was junk. In fact, "we predicted junk DNA wasn't junk" is the single leading talking point IDists have about how ID can allegedly be useful science. Now, the ID claims can be right or wrong. I am pointing out simple facts that indicate that the ID claims are wrong, because an awful lot of the DNA in many genomes looks like, basically, junk. It's unnecessary. We know this because nearly identical organisms don't have it and are just fine.NickMatzke_UD
July 15, 2011
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Born: "Hey Nick, speaking of details of science being ignored by Darwinists: Please tell me where the DNA code came from in the first place, this is a fairly significant detail:" Yes, do tell.junkdnaforlife
July 15, 2011
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Correction on my figures, although they don't change the argument: human genome = 3.5 picograms of DNA (about 3 Megabases) onion genome sizes range from 7 pg (twice the human genome size) to 31.5 (9 times the human genome size) So: why do some onions take *7 human genomes worth of DNA* **more** to build an onion that is basically similar to another onion?NickMatzke_UD
July 15, 2011
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