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Sternberg Plasters Matheson

“I think this will come to be a classic story of orthodoxy derailing objective analysis of the facts, in this case for a quarter of a century…The failure to recognize the full implications of this-particularly the possibility that the intervening noncoding sequences may be transmitting parallel information in the form of RNA molecules-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

Steve Matheson, a teacher and Darwinist promoter at a religious school, repeats the biggest mistake in molecular biology. In contrast, Richard Sternberg, an evolutionary biologist at the Biologic Institute, defends objective analysis of the facts. See Sternberg’s defense of the facts against Matheson’s Darwinist ideology in the essay: Mathesons Intron Fairytale.

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106 Responses to Sternberg Plasters Matheson

  1. Sternberg observes:

    On Friday, May 14, I watched as Steve Meyer faced his critics—two of them anyway, Art Hunt and Steve Matheson—at Biola University in Los Angeles. Matheson had previously claimed that Meyer misrepresented introns in his book, Signature in the Cell. (Introns are non-protein-coding sequences of DNA that occur within protein-coding regions.) In a blog post dated February 14, Matheson had accused Meyer of “some combination of ignorance, sloth, and duplicity” for stating in his book that although introns do not encode proteins they nevertheless “play many important functional roles in the cell.”
    Calling Meyer’s statement “ludicrous,” Matheson wrote on his blog that biologists have identified functional roles for only “a handful” of the 190,000 or so introns in the human genome:

    How many? Oh, probably a dozen, but let’s be really generous. Let’s say that a hundred introns in the human genome are known to have “important functional roles.” Oh fine, let’s make it a thousand. Well, guys, that leaves at least 189,000 introns without function.

    Matheson added that “there are more layers of duplicity in the ‘junk DNA’ fairy tale than Meyer has included in his book,” which (Matheson concluded) uses science to advance an agenda in which “rigorous scientific truth-telling is secondary.”

    Naturally, I expected Matheson to bring up this devastating criticism at the Biola event on May 14. But he said nothing about Meyer’s “ludicrous” notions of intron functions that evening, and he was mum about all the other layers of duplicity that he claims to be privy to. This was probably wise, because Matheson is wrong about intron functionality.

  2. It’s comforting to see that there are still good old darwinists whi stick to the belief that junk DNA is junk. Ah, that’s what we expect from darwinists. Not the more recent “politically correct” attitude of the type:

    “It’s obvious that non coding DNA is important for regulation and for function. Whever said differently? Neo darwinism had always predicted that”.

    So, blessed aree the Morans, the Mathesons and the like of them. Good old people, loyal to the good old nonsense.

  3. Well at least Matheson did display some honesty at one point in his exchange with Dr. Meyer, which is more than I can say for many evolutionists who disagree with Meyer, in when Dr. Matheson admitted ID had the superior case for establishing causality to the information we find embedded in life:

    here is the audio of the exchange:

    Stephen Meyer Has Even His Critics Agreeing: Intelligent Design Makes Sense
    http://www.idthefuture.com/201.....s_cri.html

    Though, I have to admit that that respect which Matheson had earned from me, for his honesty to Dr. Meyer, quickly evaporated by the less than forthright manner he handled Dr. Sternberg’s rebuttal of his 95% Junk DNA position.

  4. “It’s obvious that non coding DNA is important for regulation and for function. Whever said differently? Neo darwinism had always predicted that”.

    HAHA yea ok

  5. They predicted it while trumpeting it as a prime piece of evidence for evolution.

  6. Off topic CS Lewis radio address:

    “The lone surviving reel of audio with Lewis’s voice on it. He deals with prayer and evolution (Evolution on the second installment). Recorded during WW ll these talks eventually became “Mere Christianity”

    C.S Lewis’s surviving BBC radio address
    http://www.youtube.com/watch?v=JHxs3gdtV8A

    C.S Lewis’s surviving BBC radio address: Part 2
    http://www.youtube.com/watch?v=xYoU5_MQOU0

    Evolution Vs. The Christian Experience – cartoon video
    http://www.metacafe.com/watch/4104600

    CS Lewis song – Brooke Fraser
    http://www.youtube.com/watch?v=GHpuTGGRCbY

  7. One thing I don’t understand: these people who still believe that junk DNA is junk, how do they explain the regulatory procedures which must exist, especially in multicellular organisms?

    I find it difficult to imagine how the information for the procedures can be coded in the genome, but at least I do believe in the functional importance of all the genome, and not only of 3.5% of it (speaking of humans). So, I can always think: “we don’t know yet, but we are going to understand in time; all these introns, repetitive elements, and other mysterious sequences, must mean something. There is a lot to decode, a lot to discover”.

    But our darwinist friends, what do they really think, when they are not busy bad mouthing ID? Are they really convinced that the procedures are not written anywhere? That there is no mass memory for them? That alternative splicing happens according to alternative lucky feedbacks? That the whole development of body plans from the zygote is effectively managed by the asymetrical epigenetic information in the ovum? That each specific transcriptome for each cell type and cell state is selected from the transcriptome space by mere mechanistic events, without any informational support? That the macroscopic and microscopic structure of human central nervous system are generated by some kind of fractal mechanism, without any informational support? And so on?

    Again, where are the procedures written? Non coding DNA is an important possibility, but if they don’t believe even in that, what is left for them? Epigenetic? Confusion? Axioms?

  8. Todd Wood thinks Sternberg was unduly harsh.

  9. bevets:

    Todd Wood thinks Sternberg was unduly harsh.

    The vast majority of Dr. Sternberg’s commenst was a careful and considered recitation of the state-of-the art in dispassionate terms, with no personal animosity.

    I could find only one part of Dr. Sternberg’s response which might be considered “harsh”:

    “A job, obviously, that Matheson has not done—though whether through ignorance, sloth, or duplicity I cannot say.

    And in this he was only quoting Matheson’s original words made in reference to Dr. Meyer.

    So perhaps Todd Wood is unduly defensive.

  10. Are we all in agreement with Sternberg and Wells when they claim that every intron in every human gene whose RNAs are subject to alternative splicing are themselves alternatively spliced?

  11. Art,

    I presume you can correspond with Rick or Jonathan and get their exact position.

    I’d prefer to do that than agree or disagree with your characterization of what they assert.

  12. Arthur Hunt:

    I can certainly agree with the following claims made by me:

    a) It’s not important to know if all introns cooperate in alternative splicing, or not. According to available data, it is perfectly reasonable to assume that many, probably most, of them do.

    b) It is, in the same way, perfectly reasonable to assume that introns take part also in other regulatory functions. Although many of them may at present not be known or clarified.

    c) What is absolutely not reasonable, instead, is to stick to a model according to which more than 30% of our genome (or more than 96%, if we add all other forms of non coding DNA) is non functional. Or to pretend that there are scientific reasons to think that way. Even if there were no clues to the function of non coding DNA (which, today, is certainly not true, because those clues are rapidly accumulating), two things remain certainly true:

    1) Stating that 96% of our genome is non functional only because we don’t understand its function is, at best, an argument from ignorance, and I would say a very big and bad one. Being understood by science is not certainly the only parameter to truth, otherwise science could not go on understanding new things. You certainly understand that science works by reasonable inferences, which try to explain whta is not yet known in detail: they are called theories, and they are the stuff of which science is made.

    2) There is at least one heavy argument against the non functional model, and it is the fact that coding DNA is completely insufficient to explain what we observe in living beings: indeed, while it can explain the basic mass information for coding proteins, it explains very little of how all cellular processes are regulated and controlled in a differential way in all cell types and states, not to speak of all other complex higher level regulations. In that situation, the most reasonable assumption is that the remaining part of the genome can have an important part in all those processes we still don’t understand. That’s why all reasonable people have always believed that non coding DNA would be shown to be of regulatory importance, when unreasonable people with self-assured authority proclaimed that it was junk, probably only to support their own theories.

    Now, the crowd of “non-junk” people has certainly grown, well beyond the ID circle (maybe because facts continue to come in favour of that position?). But, as I said before, it’s reassuring to find at least some people who remain consistent with their previous errors.

  13. Sal,

    Sternberg and Wells have made their positions clear. I was asking what you thought. More generally, should I believe that the current generation of ID proponents is going to be making the same (quite mistaken) claim?

    gpuccio,

    You say:

    It’s not important to know if all introns cooperate in alternative splicing, or not. According to available data, it is perfectly reasonable to assume that many, probably most, of them do.

    What data are you speaking of? Please be specific, and explain the contradiction with data such as is found in Sultan et al. (Science 15 August 2008: 956-960):

    We observed 95% of the splicing events expected in this data set, given the current sequencing depth (Table 1) (16). We identified 4096 previously unknown splice junctions in 3106 genes, mostly called by single reads and unique to one cell type (Table 1). Many of these junctions were associated with actively transcribed genes exhibiting more exons than average, pointing to rare splicing events. Approximately 6% of all splice-junction reads identified AS events (6416 junctions in 3916 genes HEK and 5195 junctions in 3262 genes in B cells) (table S9).

    In case the terminology is not clear, these authors are stating that their data shows that 6% of all splice junctions are from AS events. This is very, very different from Sternberg’s and Wells number (100%).

    As far as the functional vs. non-functional business, there is one key fact that IDists ignore in all of this. I refer, of course, to the fact that intronic RNA is made and then thrown away. We don’t call it “junk” because we don’t know if it does anything, we call it so because it is discarded.

    (OK, OK, so maybe we should be calling it “garbage DNA” instead of “junk DNA”.)

    As I learned on the 14th of May, and in many, many past discussions, the “garbage disposal” may be a central feature of the cell, required for all manner of molecular, physiological,and organismal function, but it is not on the IDists’ radar screen.

  14. Art,

    Feel free to state what you think or link to what you may have already written.

    By the way, thanks for visiting.

    Sal

  15. Of note to “Junk DNA”;

    Astonishing DNA complexity demolishes neo-Darwinism – Alex Williams
    Not only has the ENCODE project elevated UTRs out of the ‘junk’ category, but it now appears that they are far more active 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/images/pdf.....11-117.pdf

  16. 16

    What I find surprising is that Matheson had already clarified what he meant by “Junk-DNA” not having a function in a previous blog post, which he specifically referenced in his criticism of Meyer’s statement.

    This appears to be another example of the sort of misrepresentation he was referring to.

    You can find a follow up, in which Matheson addresses both his earlier post and Sternberg’s reply here.

  17. 17

    @gpuccio (#7)

    From Matheson’s reply.

    Consider the green pufferfish. It’s a pretty interesting creature: it puffs itself up to intimidate predators. More ominously, it sports a fearsome venom called tetrodotoxin that is much beloved of neuroscientists for its ability to block sodium channels (and thus nerve conduction). And consider the marbled lungfish. It has some notably peculiar traits, most obviously the ability to breathe air.

    Just a couple of fish. The genome of the green pufferfish contains about 340 million bases. That’s a lot of bases, but the pufferfish genome is about a tenth the size of the human genome. The genome of the marbled lungfish contains about 130 billion bases. That’s about 40 times the size of the human genome. That means that the lungfish genome is almost 400 times the size of the pufferfish genome.

    If you don’t see why this is a huge problem for anyone who objects to the notion of non-functional DNA (and lots of it), then you should really lay off the Kool-Aid.

  18. well veils it seems Matheson’s whole argument, once you get past the “poor Richard” platitudes of condescension against anything related to ID, rest on the assumption that neo-Drawinists never really meant that “Junk DNA” in fact junk. Well contrary to Matheson’s disbelief and your support of that disbelief:

    Junk DNA Predictions By Evolutionists

    Selfish DNA: the ultimate parasite. Orgel LE, Crick FH.
    The DNA of higher organisms usually falls into two classes, one specific and the other comparatively nonspecific. It seems plausible that most of the latter originates by the spreading of sequences which had little or no effect on the phenotype. http://www.ncbi.nlm.nih.gov/pubmed/7366731

    Kimura (1968) developed the idea of “Neutral Evolution”. If “Haldane’s Dilemma” is correct, the majority of DNA must be non-functional.

    The slow, painful death of junk DNA:
    Junk DNA is not just a label that was tacked on to some DNA that seemed to have no function; it is something that is required by evolution. Mathematically, there is too much variation, too much DNA to mutate, and too few generations in which to get it all done. This was the essence of Haldane’s work….Junk DNA is a necessary mathematical extrapolation…Without Junk DNA, evolution runs into insurmountable mathematical difficulties. http://creation.com/junk-dna-slow-death

    Susumu Ohno, a leader in the field of genetics and evolutionary biology, explained in 1972 in an early study of non-coding DNA that, “they are the remains of nature’s experiments which failed. The earth is strewn with fossil remains of extinct species; is it a wonder that our genome too is filled with the remains of extinct genes?”

    In 1994, the authoritative textbook, Molecular Biology of the Cell, co-authored by National Academy of Sciences president Bruce Alberts, suggested (incorrectly!) that introns are “largely genetic ‘junk’”: Unlike the sequence of an exon, the exact nucleotide sequence of an intron seems to be unimportant. Thus introns have accumulated mutations rapidly during evolution, and it is often possible to alter most of an intron’s nucleotide sequence without greatly affecting gene function. This has led to the suggestion that intron sequences have no function at all and are largely genetic “junk”

    Soon thereafter, the 1995 edition of Voet & Voet’s Biochemistry textbook explained that “a possibility that must be seriously entertained is that much repetitive DNA serves no useful purpose whatever for its host. Rather, it is selfish or junk DNA, a molecular parasite that, over many generations, has disseminated itself throughout the genome…”

    Will Darwinists try to Rewrite the History of Junk-DNA?
    In 1996, leading origin of life theorist Christian de Duve wrote: “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.” (Richard Dawkins makes similar pronouncements that DNA is junk in an article after 1998) http://www.evolutionnews.org/2.....ull_a.html

    Another leading biologist, Sydney Brenner argued in a biology journal in 1998 that:
    “The excess DNA in our genomes is junk, and it is there because it is harmless, as well as being useless, and because the molecular processes generating extra DNA outpace those getting rid of it.”

    The Unseen Genome, Gems Among the Junk:
    “I think this will come to be a classic story of orthodoxy derailing objective analysis of the facts, in this case for a quarter of a century,” Mattick says. “The failure to recognize the full implications of this—particularly the possibility that the intervening noncoding sequences may be transmitting parallel information in the form of RNA molecules—may well go down as one of the biggest mistakes in the history of molecular biology.” (John S. Mattick Scientific American (November, 2003) http://www.evolutionnews.org/

  19. veils @ 16, lets get into the whole c-value enigma a little bit here:

    C-value enigma
    Excerpt: it was soon found that C-values (genome sizes) vary enormously among species and that this bears no relationship to the presumed number of genes (as reflected by the complexity of the organism). For example, the cells of some salamanders may contain 40 times more DNA than those of humans. Given that C-values were assumed to be constant because DNA is the stuff of genes, and yet bore no relationship to presumed gene number, this was understandably considered paradoxical; http://en.wikipedia.org/wiki/C-value_enigma

    Thus the finding of enormously varying genome sizes is actually a failed prediction of evolutionary theory since the materialistic presuppositions, under-girding neo-Darwinism, predicted there to be a correlation between genome sizes and macroscopic complexity of the species. That neo-Darwinists would try to twist this failed prediction of materialism around to argue that it supports the ludicrous claim of Junk DNA, despite the finding of large scale functionality in so called “junk” regions, is another prime example of a theory that is completely divorced from any empirical falsification whatsoever.

  20. If you don’t see why this is a huge problem for anyone who objects to the notion of non-functional DNA (and lots of it), then you should really lay off the Kool-Aid.

    THe problem is that just because Matheson can’t perceive the function he presumes there is no function. Utter stupidity!

    DNA is not only for coding! Just because it is not obviously utilized for coding does not mean it has no use. The use may yet be discovered.

    Examples 1: non-coding DNA for lenses

    Shoddy Engineering or Intelligent Design? Case of the Mouse’s Eye

    We often hear from Darwinians that the biological world is replete with examples of shoddy engineering, or, as they prefer to put it, bad design. One such case of really poor construction is the inverted retina of the vertebrate eye. As we all know, the retina of our eyes is configured all wrong because the cells that gather photons, the rod photoreceptors, are behind two other tissue layers. Light first strikes the ganglion cells and then passes by or through the bipolar cells before reaching the rod photoreceptors. Surely, a child could have arranged the system better — so they tell us.

    The problem with this story of supposed unintelligent design is that it is long on anthropomorphisms and short on evidence. Consider nocturnal mammals. Night vision for, say, a mouse is no small feat. Light intensities during night can be a million times less than those of the day, so the rod cells must be optimized — yes, optimized — to capture even the few stray photons that strike them. Given the backwards organization of the mouse’s retina, how is this scavenging of light accomplished? Part of the solution is that the ganglion and bipolar cell layers are thinner in mammals that are nocturnal. But other optimizations must also occur. Enter the cell nucleus and “junk” DNA.

    Only around 1.5 percent of mammalian DNA encodes proteins. Since it has become lore to equate protein-coding regions of the genome with “genes” and “information,” the remaining approximately 98.5 percent of DNA has been dismissed as junk. Yet, for what is purported to be mere genetic gibberish, it is strikingly ordered along the length of the chromosome. Like the barcodes on consumer items that we are all familiar with, each chromosome has a particular banding pattern. This pattern reflects how different types of DNA sequences are linearly distributed. The “core” of a mammalian chromosome, the centromere, and the genomic segments that frame it largely consist of long tracks of species-specific repetitive elements — these areas give rise to “C-bands” after a chemical stain has been applied. Then, alternating along the chromosome arms are two other kinds of bands that appear after different staining procedures. One called “R-bands” is rich in protein-coding genes and a particular class of retrotransposon called SINEs (for Short Interspersed Nuclear Elements). SINE sequence families are restricted to certain taxonomic groups. The other is termed “G-bands” and it has a high concentration of another class of retrotransposon called LINEs (for Long Interspersed Nuclear Elements), that can also be used to distinguish between species. Finally, the ends of the chromosome, telomeres, are comprised of a completely different set of repetitive DNA sequences.
    In general, C-bands and G-bands are complexed with proteins and RNAs to give a more compact organization called heterochromatin, whereas R-bands have a more open conformation referred to as euchromatin.

    Why bother with such details? Well, each of these chromosome bands has a preferred location in the cell nucleus. Open any good textbook on mammalian anatomy and you will note that cell types can often be distinguished by the shape and size of the nucleus, as well as the positions of euchromatin and heterochromatin in that organelle. Nevertheless, most cell nuclei follow a general rule where euchromatin is located in the interior, in various compartments that are dense with transcription factories, RNA processing machinery, and many other components. Heterochromatin, on the other hand, is found mainly around the periphery of the nucleus. A striking exception to this principle is found in the nuclei of rod cells in nocturnal mammals.

    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.

  21. Example 2, “junk” DNA used as qudruplex “organelles”:

    Guy Walks Into a Bar and Thinks He’s a Chimpanzee: The Unbearable Lightness of Chimp-Human Genome Similarity

    At this break, three things happen. The bartender receives my nod that I want another drink and then, after he places it before me, I inquire as to whether he can play anything by Ethel Ennis — I now want to listen to something languorous, music that will soothe the feeling of ennui that has come over me. Next, or simultaneously, my sparring partner makes one of two moves. Either he places his book into his hand-woven Inca-nesque bag and leaves without so much as a farewell, or he decides to tarry a bit longer and says, “You have no answer for ITSs, do you?”

    ITSs…interstitial telomeric sequences…the chromosome scars, the pieces of junk DNA he was lecturing me about earlier. As you know, telomeres are the ends of chromosomes. In many species, including chimps and humans, the DNA sequences that are found at these genomic tips are tandem repetitions of TTAGGG. That’s right…TTAGGGTTAGGGTTAGGG…over and over and over again. A notable exception to this rule is the fruit fly, an organism that in this regard has provided the junk DNA notion no succor, since its telomeres have complex combinations of three different retrotransposons instead of those six-basepair units. What is important to note, though, is that telomeric sequences are essential to the cell, and it seems that hardly a week does not pass without some new role being discovered for these elements.

    How, precisely, are miles and miles of TTAGGG of significance? From the standpoint of chromosome architecture, the repetitive elements en masse have the propensity to form complicated topologies such as quadruplex DNA. These sequences or, rather, topographies are also bound by a host of chromatin proteins and particular RNAs to generate a unique “suborganelle” — for the lack of better term — at each end. As a matter of fact, the chromatin organization of telomeres can silence genes and has been linked to epigenetic modes of inheritance in yeast and fruit flies. Furthermore, different classes of transcripts emanate from telomeres and their flanking repetitive DNA regions, which are involved in various and sundry cellular and developmental operations.

    I try to outline all the functions of telomeric repeats, but my friend tells me that I am getting off the subject.

    He wants to me to focus on the ITSs, the tracks of the hexamer TTAGGG that reside within chromosome arms or around the centromere, not at the ends. I tell him that I was just coming to that topic. The story, you see, is that in the lineage leading up (or down, I forget which) to chimps and humans, a fusion of chromosome ends occurred — two telomeres became stuck together, the DNA was stitched together, and now we find the remnants of this event on the inside of chromosomes. And to be fair, I concede at this point that the 2q13 ITS site shared by chimps and humans can be considered a synapomorphy, a five-dollar cladistic term meaning a genetic marker that the two species share. As this is said, it is apparent that the countenance of my acquaintance lightens a bit only to darken a second later. For I follow up by saying that of all the known ITSs, and there are many in the genomes of chimps and humans, as well as mice and rats and cows…, the 2q13 ITS is the only one that can be associated with an evolutionary breakpoint or fusion. The other ITSs, I hasten to add, do not square up with chromosomal breakpoints in primates (Farré M, Ponsà M, Bosch M. 2009. “Interstitial telomeric sequences (ITSs) are not located at the exact evolutionary breakpoints in primates,” Cytogenetic and Genome Research 124(2): 128-131.). In brief, to hone in on the 2q13 ITS as being typical of what we see in the human and chimp genomes seems almost like cherry-picking data. Most are not DNA scars in the way they have been portrayed.

    Exasperated with my stubbornness, the caffeine from innumerable herbal teas having only enhanced his tension, he rises from the bar and asks: “How, then, do you account for such ITSs in the first place…everyone knows they are out-of-place junk.” I tell him that I do have an answer but that first I must be excused for a moment. While making my way back to the bar, I mentally rehearse so as to be as succinct as possible. My rejoinders are, simply, that ITSs reflect sites where TTAGGG repeats have been added to chromosomes by telomerases, that these repeats are moreover engineered — literally synthesized by the telomerase machinery, that ITSs have a telomere-like chromatin organization and are associated with distinct sets of proteins, and that many have been linked to roles such a recombination hotspots. And just as I begin to reflect on where the references are in my bag that supports those points I notice…he is gone.

  22. Sal, I really like those references: Let’s not forget the paper that Dr. Sternberg referenced:

    Canadian Team Develops Alternative Splicing Code from Mouse Tissue Data
    Excerpt: “Our method takes as an input a collection of exons and surrounding intron sequences and data profiling how those exons are spliced in different tissues,” Frey and his co-authors wrote. “The method assembles a code that can predict how a transcript will be spliced in different tissues.”
    http://www.genomeweb.com/infor.....issue-data

    Thus the fairly stunning success at which they were able to predict alternative splicing in different tissues was directly dependent of presupposing the intron sequences to be functional. Whereas Matheson would not have even have been “in the ballpark” for trying to figure out the alternative splicing code since he so drastically presupposes non-functionality for intron sequences.

  23. Matheson:

    Consider the green pufferfish. It’s a pretty interesting creature: it puffs itself up to intimidate predators. More ominously, it sports a fearsome venom called tetrodotoxin that is much beloved of neuroscientists for its ability to block sodium channels (and thus nerve conduction). And consider the marbled lungfish. It has some notably peculiar traits, most obviously the ability to breathe air.

    Just a couple of fish. The genome of the green pufferfish contains about 340 million bases. That’s a lot of bases, but the pufferfish genome is about a tenth the size of the human genome. The genome of the marbled lungfish contains about 130 billion bases. That’s about 40 times the size of the human genome. That means that the lungfish genome is almost 400 times the size of the pufferfish genome.

    If you don’t see why this is a huge problem for anyone who objects to the notion of non-functional DNA (and lots of it), then you should really lay off the Kool-Aid.

    i.e., argument from ignorance.

    I understand the apparent problem, but I also know that this same statement could have a couple of the facts replaced and it would be identical to a typical statement a couple decades ago, which are now becoming more and more fallacious with each molecular biology discovery, it seems.

    With what it seems that we don’t know about regulation and expression on the molecular level in biology, the less convincing this argument is to me.

    I’m still waiting for the evidence or model that makes it remotely reasonable to expect law and chance, devoid of intelligence, to create functional, complex, specified information, at least within the probabilistic resources of the history of the known Universe. Until then, functional “junk” DNA, marvelous engineering wonders in biology that trump anything humans have created, consciousness, etc. are simply circumstantial evidence, comparatively. It seems that if one is determined to believe in naturalism, they could dream up stories that could possibly fill those voids, but there is no cheating statistics.

  24. Just because DNA doesn’t code for something, are we justified in presuming it’s junk?

    INTEL chips on computers large amounts of casing that have no apparent computational use. In fact the casing looks excessively large. It seems to provide no structural benefit. They don’t provide any memory or information (coding if you will). Do we deem it useless “junk” since it doesn’t code for anything? NO. If functions as a heat sink and radiator, and prevents the chip melting!

    But junk advocate Darwinsits like Matheson resort to about the same level of twisted reasoning regarding DNA. Just because DNA doesn’t code for something, they presume it’s junk! That would be about as stupid as saying because the heat sink in a computer chip doesn’t provide any computation, it is junk.

    I provided examples where DNA is used for other purposes than coding. The repetitive nature of the DNA in certain cases is essential for functioning, but because of the propenesity to label anything that doesn’t code as junk, science and understanding have been hindered.

    Maybe the prejudicial view of pufferfish genomes is preventing exploration of the real function of the DNA.

  25. Here is Dr. Sternberg on ERV’s

    Refutation Of Endogenous Retrovirus – Richard Sternberg PhD. – video
    http://www.metacafe.com/watch/.....nberg_phd/

    further notes:

    No Such Thing As ‘Junk RNA,’ Say Researchers – Oct. 2009
    Excerpt: Tiny strands of RNA previously dismissed as cellular junk are actually very stable molecules that may play significant roles in cellular processes, http://www.sciencedaily.com/re.....105809.htm

    Excerpt Of Conclusion:
    When examined in detail, the full pseudogene dataset we collected does not lend itself to a reasonable neo-Darwinian interpretation.
    http://creation.com/images/pdf.....18-127.pdf

    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, speaking of the gene regulation was a straightforward, linear process of gene coding for regulator protein that controls transcription. “Biology’s new glimpse at a universe of non-coding DNA – what used to be called ‘junk’ DNA – has been fascinating and befuddling.” If it’s junk, why would the human body decode 74% to 93& of it? The plethora of small RNAs produced by these non-coding regions, and how they interact with each other and with DNA, was completely unexpected when the project began.,,,
    http://www.creationsafaris.com.....#20100405a

    All Proposed Elements Of Junk DNA have been Found To Have High Level Function – assorted studies
    http://docs.google.com/View?id=dc8z67wz_25gqm4zzfd

  26. Off-topic,

    This researcher puts technological innovations into nested hierarchies.

    http://www.iir.hit-u.ac.jp/iir.....nested.pdf

  27. If Matheson, Hunt, Moran and company entertain any doubts that the Junk DNA mindset had anything whatsoever to do with unraveling the “second code”, here is the proof that the team totally disregarded neo_Darwinian thinking:

    Researchers Crack ‘Splicing Code,’ Solve a Mystery Underlying Biological Complexity – May 2010
    Excerpt: Frey and Blencowe attribute the success of their project to the close collaboration between their team of talented computational and experimental biologists. “Understanding a complex biological system is like understanding a complex electronic circuit. Our team ‘reverse-engineered’ the splicing code using large-scale experimental data generated by the group,” Frey said.
    http://www.sciencedaily.com/re.....133252.htm

  28. Further note on Junk DNA:

    Darwinists clinging to the Junk DNA paradigm is against reason and more importantly is also now shown to be against current experimental evidence:

    Arriving At Intelligence Through The Corridors Of Reason (Part II) – April 2010
    Excerpt: In fact the term ‘junk DNA’ is now seen by many an expert as somewhat of a misnomer since much of what was originally categorized as such has turned out to be pivotal for DNA stability and the regulation of gene expression. In his book Nature’s Probability And Probability’s Nature author Donald Johnson has done us all a service by bringing these points to the fore. He further notes that since junk DNA would put an unnecessary energetic burden on cells during the process of replication, it stands to reason that it would more likely be eliminated through selective pressures. That is, if the Darwinian account of life is to be believed. “It would make sense” Johnson writes “that those useless nucleotides would be removed from the genome long before they had a chance to form something with a selective advantage….there would be no advantage in directing energy to useless structures”.
    http://www.uncommondescent.com.....n-part-ii/

    These following studies back up this assertion:

    Experimental Evolution of Gene Duplicates in a Bacterial Plasmid Model
    Excerpt: In a striking contradiction to our model, no such conditions were found. The fitness cost of carrying both plasmids increased dramatically as antibiotic levels were raised, and either the wild-type plasmid was lost or the cells did not grow. This study highlights the importance of the cost of duplicate genes and the quantitative nature of the tradeoff in the evolution of gene duplication through functional divergence.
    http://www.springerlink.com/co.....4014664w8/

    Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness – May 2010
    Excerpt: Despite the theoretical existence of this short adaptive path to high fitness, multiple independent lines grown in tryptophan-limiting liquid culture failed to take it. Instead, cells consistently acquired mutations that reduced expression of the double-mutant trpA gene. Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken.
    http://bio-complexity.org/ojs/.....O-C.2010.2

  29. 29

    @scordova (#19)

    Scordova,

    I’m having a difficult time understanding your responses given the numerous clarifications Matheson has presented.

    Are you…

    A. Objecting to the notion of “junk-DNA” in principal?

    B. Suggesting that Matheson is somehow ignorant of “functions” that “junk-DNA” has?

    C. Suggesting a lack of imagination on Matheson part?

    For examle, Matheson has already addressed [A] on multiple occasions, including a suggestion that the term “Junk-DNA” is a unfortunate choice of words.

    But even then, a few of the items in my home would qualify as “junk”, despite the fact that they may perform their original purpose and their value is purely sentimental. To other people, these items are “junk.” However, I in no way object or to nor am I offended by the use of the word because I understand the context in which is it’s used.

    To quote Matheson’s translation of Sternberg’s post….

    Paint cans are sometimes found in piles of rubbish in vacant urban lots (VULs). Paint cans can be used to prop up old cars, or to fight off intruders, or to make music. Therefore VULs are useful in auto repair, home security, and musical composition.

    Given the generous number of clarifications presented, could it be that your simply find the term “junk” offensive?

    In regards to [B], Matheson clearly addressed this issue in his reply which I’ll defer to rather than quote here.

    In other words, you seem to be presenting arguments which Matheson has already addressed, which again makes me think you’re simply offended by the use of term, despite multiple clarifications.

  30. 30

    @ bornagain77

    You wrote:

    Thus the finding of enormously varying genome sizes is actually a failed prediction of evolutionary theory

    You’re referring to the C-paradox, which was resolved via the discovery that some of an organism’s genome is non-coding. That is, areas are not directly involved in coding.

    What remains is the C-value enigma, which reflects our lack of understanding of non-coding DNA in a number of areas…

    - How prevalent is non-coding DNA in other biological organisms?
    - Where does non-coding DNA come from and what determines it’s transfer (or lack there of) over time?
    - What other functions might non-coding DNA have in other areas?
    - Why doe the amount of non-coding DNA vary greatly between organisms?

    However, none of these questions negate Matheson’s point.

    To repeat, what “function” are these 127 billon bases performing in a Lungfish that are not being performed in a Human Being? We can ask the same about the 129+ billion bases not found in a Pufferfish.

    @uoflcard

    You wrote:

    i.e., argument from ignorance.

    But then wrote:

    I’m still waiting for the evidence or model that makes it remotely reasonable to expect law and chance, devoid of intelligence, to create functional, complex, specified information, at least within the probabilistic resources of the history of the known Universe.

    Should I assume you’re just as open to the idea that the possible “functions” of non-coding DNA could resolve many if not all of the supposedly insurmountable problems you’ve just mentioned?

    @scordova (#24)

    You wrote:

    Maybe the prejudicial view of pufferfish genomes is preventing exploration of the real function of the DNA.

    It seems you’ve made an argument that was both predicted and addressed in Matheson’s response. See the article he referenced here.

  31. veils; the c-value paradox is most assuredly NOT resolved within the materialistic framework, despite your very forgiving attitude towards the Darwinian materialistic foundation in science. This is because information is presupposed to “emerge” from a material basis; the non-correlation of genome size to the apparent complexity witnessed in life is a “surprise” since the material basis of the genome is suppose to have a fairly linear correlation to the information “emerging” from it, whereas in Intelligent Design the genome size is first presupposed to be directly dependent of functional optimality, as was amply illustrated by Sal here:

    “Junk DNA” is found to have purpose in an astonishing way in this following paper:

    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/2......html#more

    It is clear from this study, by itself, that your presupposition of “paint cans and junk cars” is vastly to simplistic.

  32. v wrote:

    It seems you’ve made an argument that was both predicted and addressed in Matheson’s response. See the article he referenced here.

    To quote Matheson:

    Matheson writes:

    Junkyards, after all, contain lots of stuff that can serve a function

    Finding utility in junkyard parts can be argued as evidence of innovation. So the label of “junk” is only prejudicial, it hardly argues against design.

    By Mathesons reasoning, the fact that a car may have a part that came from a junk yard some how disqualifies the rebuilt car from being desinged?

    The label of “junk” is only prejudicial, and even if it were junk, it hardly refutes the design hypothesis.

    There is something beautiful to be said about turning what is bad into something good, or does Matheson want to argue God recreating something that was bad into something is evidence God is not as smart as Matheson? :-)

    NOTE:

    I’m not saying the DNA is junk, I’m saying, even it you labeled it as such, it doesn’t refute the design hypothesis.

  33. Matheson:

    And I hope it’s a little clearer what I mean when I say that introns aren’t known to be functional. Sternberg was wrong to assume that I would share his view of what it means for something to have “function,” and he was doubly wrong to think that I would predict that introns don’t sometimes – even often – contain elements that serve functional roles. Junkyards, after all, contain lots of stuff that can serve a function. (My previous attempt to illustrate this concept employed Yugos. Check it out. Todd Wood liked it too.)

    Sounds more like someone embarassed to admit his error after being called on it. :-)

  34. Are we all in agreement with Sternberg and Wells when they claim that every intron in every human gene whose RNAs are subject to alternative splicing are themselves alternatively spliced?

    Art,

    I don’t agree that is their claim, that is your characterization of what they said. We’ll have to hear it from them before I agree.

    Sal

  35. v asked:

    Scordova,

    I’m having a difficult time understanding your responses given the numerous clarifications Matheson has presented.

    Are you…

    A. Objecting to the notion of “junk-DNA” in principal?

    B. Suggesting that Matheson is somehow ignorant of “functions” that “junk-DNA” has?

    C. Suggesting a lack of imagination on Matheson part?

    For examle, Matheson has already addressed [A] on multiple occasions, including a suggestion that the term “Junk-DNA” is a unfortunate choice of words

    I’m objecting to his inept line of reasoning:

    Example of Matheson Reasoning:

    Let’s say that a hundred introns in the human genome are known to have “important functional roles.” Oh fine, let’s make it a thousand. Well, guys, that leaves at least 189,000 introns without function.

    So according to Matheson, if a function has not been discovered in an intron, it is deemed functionless by default. Stupidity times 10! I’d expect more from a sceintist examing complex systems.

  36. Sal, here is what Sternberg says:

    So let’s do the math. Again. I will make the task easy for everyone—even Moran and Matheson:

    Step 1. There are ~25,000 protein-coding genes in the human genome.

    Step 2. There are 190,000 introns/25,000 protein-coding genes = 7.6 introns/gene on average.

    Step 3. Ninety percent (possibly more) of gene transcripts undergo alternative splicing. Hence, 0.9 x 25,000 = 22,500 genes (actually, their RNAs) undergo alternative splicing.

    Therefore, 22,500 genes x 7.6 introns/gene = 171,000 introns involved in alternative splicing.

    What else can this mean but that every one of the 7.6 introns in every gene that is subject to alternative splicing are themselves alternatively spliced? I think Sternberg is quite clear about this.

    Clear, and completely wrong.

  37. 37

    scordova,

    This isn’t much of an improvement as you’ve simply reproduced the original quote and essentially made the same objection.

    You wrote I’m objecting to his inept line of reasoning:

    While I’m not trying to create a false dilemma, it seems you could only reach this conclusion by pointing out a specific error in his reasoning, rather than saying it’s inept. Right?

    You wrote:

    So according to Matheson, if a function has not been discovered in an intron, it is deemed functionless by default. Stupidity times 10! I’d expect more from a sceintist examing complex systems.

    Are you suggesting that his reasoning breaks down, but in a way that none of the options I presented are relevant? If so, then kindly explain why his reasoning is “Stupidly times 10!” without appealing to any of them.

    For example, it seems obvious that context in which the term functionless was used is highly relevant in deterring if Matheson’s reasoning was inept. Wouldn’t you agree? But, again, Matheson’s post included clear examples of what he meant by functionless. And he did so because he expected this sort of reaction from ID supporters.

    Could it be that you simply didn’t want to disappoint him?

  38. 38

    @scordova (#32)

    My comment was referring to your suggestion that “propenesity to label anything that doesn’t code as junk, science and understanding have been hindered.” was expected and had already been addressed elsewhere. Yet you chose to make the argument anyway.

    You changed the subject when you wrote;

    You wrote:

    Finding utility in junkyard parts can be argued as evidence of innovation. So the label of “junk” is only prejudicial, it hardly argues against design.

    So, I should assume [A] you object to the notion of “junk-DNA” in principal, because it’s prejudicial? Again, it sounds like you’re offended by the term, rather that confused about the context in which Matheson used it.

    Let me guess, God doesn’t make “junk” and you couldn’t possible imagine that the entirety of DNA wasn’t specifically planned by God?

    By Mathesons reasoning, the fact that a car may have a part that came from a junk yard some how disqualifies the rebuilt car from being designed?

    It’s unclear how you reached this conclusion or how this is relevant to your suggestion that using the term “junk-DNA” in conduction with non-coding DNA as has somehow harmed science. Care to respond to the responses provided?

  39. you know veilsofmaya, not to interrupt your ironing out over the precise meaning of Junk with sal, but I hope you can help me with this one particular problem that a lot of ID proponents can’t get past,,, You see veilsofmaya the problem is that no neo-Darwinists has ever demonstrated that material processes can generate any functional information whatsoever!!! NOT EVEN ONE TIME!!! And yet the genome of the simplest organism on earth is vastly more complex in its programming complexity that any computer program ever written by man. I hope you can see my concern. You see you are sitting here arguing that what you mean by junk don’t really mean what i mean by junk and yet this junk. however you want to look at it, is vastly superior to programs written by teams of our best engineers. All I can say is,,, Man that is some kind of junk you got there no matter what you want to call it!!! So if, after you take care of that important junk definition thing, you could get around to falsifying Abel’s null hypothesis for information generation I would appreciate it:

    notes:

    “No man-made program comes close to the technical brilliance of even Mycoplasmal genetic algorithms. Mycoplasmas are the simplest known organism with the smallest known genome, to date. How was its genome and other living organisms’ genomes programmed?” – David L. Abel and Jack T. Trevors, “Three Subsets of Sequence Complexity and Their Relevance to Biopolymeric Information,” Theoretical Biology & Medical Modelling, Vol. 2, 11 August 2005, page 8 http://www.biomedcentral.com/c.....2-2-29.pdf

    The Capabilities of Chaos and Complexity: David L. Abel – Null Hypothesis For Information Generation – 2009
    To focus the scientific community’s attention on its own tendencies toward overzealous metaphysical imagination bordering on “wish-fulfillment,” we propose the following readily falsifiable null hypothesis, and invite rigorous experimental attempts to falsify it: “Physicodynamics cannot spontaneously traverse The Cybernetic Cut: physicodynamics alone cannot organize itself into formally functional systems requiring algorithmic optimization, computational halting, and circuit integration.” A single exception of non trivial, unaided spontaneous optimization of formal function by truly natural process would falsify this null hypothesis.
    http://www.mdpi.com/1422-0067/10/1/247/pdf
    Can We Falsify Any Of The Following Null Hypothesis (For Information Generation)
    1) Mathematical Logic
    2) Algorithmic Optimization
    3) Cybernetic Programming
    4) Computational Halting
    5) Integrated Circuits
    6) Organization (e.g. homeostatic optimization far from equilibrium)
    7) Material Symbol Systems (e.g. genetics)
    8) Any Goal Oriented bona fide system
    9) Language
    10) Formal function of any kind
    11) Utilitarian work
    http://mdpi.com/1422-0067/10/1/247/ag

    First-Ever Blueprint of ‘Minimal Cell’ Is More Complex Than Expected – Nov. 2009
    Excerpt: A network of research groups,, approached the bacterium at three different levels. One team of scientists described M. pneumoniae’s transcriptome, identifying all the RNA molecules, or transcripts, produced from its DNA, under various environmental conditions. Another defined all the metabolic reactions that occurred in it, collectively known as its metabolome, under the same conditions. A third team identified every multi-protein complex the bacterium produced, thus characterising its proteome organisation.
    “At all three levels, we found M. pneumoniae was more complex than we expected,”
    http://www.sciencedaily.com/re.....173027.htm

    Simplest Microbes More Complex than Thought – Dec. 2009
    Excerpt: PhysOrg reported that a species of Mycoplasma,, “The bacteria appeared to be assembled in a far more complex way than had been thought.” Many molecules were found to have multiple functions: for instance, some enzymes could catalyze unrelated reactions, and some proteins were involved in multiple protein complexes.”
    http://www.creationsafaris.com.....#20091229a

    Human DNA is like a computer program but far, far more advanced than any software we’ve ever created.
    Bill Gates, The Road Ahead, 1996, p. 188

    The Coding Found In DNA Surpasses Man’s Ability To Code – Stephen Meyer – video
    http://www.metacafe.com/watch/4050638

    Bill Gates, in recognizing the superiority found in Genetic Coding, compared to the best computer coding we now have, has now funded research into this area:

    Welcome to CoSBi – (Computational and Systems Biology)
    Excerpt: Biological systems are the most parallel systems ever studied and we hope to use our better understanding of how living systems handle information to design new computational paradigms, programming languages and software development environments. The net result would be the design and implementation of better applications firmly grounded on new computational, massively parallel paradigms in many different areas.
    http://www.cosbi.eu/index.php/.....rticle/171

    DNA Optimized for Photostability
    Excerpt: These nucleobases maximally absorb UV-radiation at the same wavelengths that are most effectively shielded by ozone. Moreover, the chemical structures of the nucleobases of DNA allow the UV-radiation to be efficiently radiated away after it has been absorbed, restricting the opportunity for damage.
    http://www.reasons.org/dna-soaks-suns-rays

    etc..etc..etc…

  40. Let’s say that a hundred introns in the human genome are known to have “important functional roles.” Oh fine, let’s make it a thousand. Well, guys, that leaves at least 189,000 introns without function.

    So do you agree that there is a specific error in his reasoning?

    Or are you going to defend his statement:

    Let’s say that a hundred introns in the human genome are known to have “important functional roles.” Oh fine, let’s make it a thousand. Well, guys, that leaves at least 189,000 introns without function.

    The inference he makes:

    “we know only a few functions for introns, therefore the rest do not have functions”.

    Consider an engineering student assigned to evaluate a piece of hardware whose documentation is now lost. What if that student said, “we don’t know the function, therefore it has none”.

    Is that sort of reasoning worthy of a student the sciences?

    v:

    Care to respond to the responses provided?

    only if you respond to my question above. Has matheson made a wrong inference here:

    Let’s say that a hundred introns in the human genome are known to have “important functional roles.” Oh fine, let’s make it a thousand. Well, guys, that leaves at least 189,000 introns without function.

    If you agree he has made an error, on a scale of stupidity, how would you rate such logic.

  41. @scordova (#39)

    Scordova,

    I’ve asked a simple question, which I think is clear, reasonable and highly relevant. I won’t ask it again.

    Nor am I interested in further discussion should you decline.

    However, if Matheson’s reasoning really is that stupid, you should have no problem pointing exactly where the problem is, right?

    For example, you might say that his reasoning was “stupid” because these introns really do have a “function.” But, Matheson has written much about the subject on his blog.

    To quote from the directly linked post, which was part two of a two part series on “Junk DNA”…

    [...] nor have biologists ever assumed universal non-function of non-coding DNA in the first place.

    You might suggest that Matheson was ignorant about the function of introns, not only in regard to Meyer’s claim but in regards to Sternberg’s post as well. However, this too was addressed here and here.

    So, I’m still left wondering exactly where is the blunder that makes this reasoning so stupid.

    While I’m under no illusion that you are somehow obliged to answer the question, your lack of response suggests that you’re simply offended by the term “Junk DNA”, despite the fact that ID is supposedly a scientific theory in that it makes no specific claim about who the designer is.

  42. I’ve asked a simple question, which I think is clear, reasonable and highly relevant. I won’t ask it again.

    Nor am I interested in further discussion should you decline.

    I’m attempting to answer, but I’ll have a better idea of how to answer your question if you can tell me whether you think the following assertion by Matheson is a correct logical inference:

    Let’s say that a hundred introns in the human genome are known to have “important functional roles.” Oh fine, let’s make it a thousand. Well, guys, that leaves at least 189,000 introns without function.

    Translation: Matheson doesn’t know that an intron has function, therefore in his mind if it is not yet known to have function it doesn’t have function.

    Is that a logical deduction? Would we go about studying human physiology and say, “we don’t know if the appendix has function, therefore the appendix is useless”.

    If we were to do science by deeming something functionless because the function was not perceived, how could we ever expect to perceive it if indeed it is there. That’s willful blindness.

    Notice, Matheson is not saying, “we don’t yet know if it has function” rather he asserts:

    Let’s say that a hundred introns in the human genome are known to have “important functional roles.” Oh fine, let’s make it a thousand. Well, guys, that leaves at least 189,000 introns without function.

    He rules out possibility of function because it is not perceived. This is bad logic.

    V:

    So, I’m still left wondering exactly where is the blunder that makes this reasoning so stupid.

    I quoted it to you several times, or do you believe the following is evidence of Matheson’s deep insight. :-)

    Let’s say that a hundred introns in the human genome are known to have “important functional roles.” Oh fine, let’s make it a thousand. Well, guys, that leaves at least 189,000 introns without function.

    C’mon V, are you going to defend that statement or call it for what it is. Are you going to claim, as Matheson suggests, that because a function has not been discovered for an intron, it has no function.

    For example, you might say that his reasoning was “stupid” because these introns really do have a “function.”

    NO! He is making a non-sequitur! The existence of function is independent of our knowledge of its existence.

    His conclusion:

    “that leaves at least 189,000 introns without function.”

    Does not follow from the premise:

    “Let’s say that a hundred introns in the human genome are known to have “important functional roles.”

    This is illogical. This is like saying, “I don’t know what function this part has in the space shuttle, therefore this part is useless.”

    A human is arguably more complex than a space shuttle. How presumptuous then to assert something has no function merely because function hasn’t been perceived yet. Lack of perceiving function in an intron is not the same as the intron having no functon. But that is Mathesonian reasoning, and he uses the same illogic with pufferfish!

  43. Mattick’s analysis:

    The Role of Introns and Other Noncoding RNAs in the Development of Complex Organisms

    Eukaryotic phenotypic diversity arises from multitasking of a core proteome of limited size. Multitasking is routine in computers, as well as in other sophisticated information systems, and requires multiple inputs and outputs to control and integrate network activity. Higher eukaryotes have a mosaic gene structure with a dual output, mRNA (protein-coding) sequences and introns, which are released from the pre-mRNA by posttranscriptional processing. Introns have been enormously successful as a class of sequences and comprise up to 95% of the primary transcripts of protein-coding genes in mammals. In addition, many other transcripts (perhaps more than half) do not encode proteins at all, but appear both to be developmentally regulated and to have genetic function. We suggest that these RNAs (eRNAs) have evolved to function as endogenous network control molecules which enable direct gene-gene communication and multitasking of eukaryotic genomes. Analysis of a range of complex genetic phenomena in which RNA is involved or implicated, including co-suppression, transgene silencing, RNA interference, imprinting, methylation, and transvection, suggests that a higher-order regulatory system based on RNA signals operates in the higher eukaryotes and involves chromatin remodeling as well as other RNA-DNA, RNA-RNA, and RNA-protein interactions. The evolution of densely connected gene networks would be expected to result in a relatively stable core proteome due to the multiple reuse of components, implying that cellular differentiation and phenotypic variation in the higher eukaryotes results primarily from variation in the control architecture. Thus, network integration and multitasking using trans-acting RNA molecules produced in parallel with protein-coding sequences may underpin both the evolution of developmentally sophisticated multicellular organisms and the rapid expansion of phenotypic complexity into uncontested environments such as those initiated in the Cambrian radiation and those seen after major extinction events.

    I’d take Mattick research over Matheson illogical speculations.

  44. Mattick points out here:

    http://ai.stanford.edu/~serafi.....RG2004.pdf

    The nematode worm Caenorhabditis elegans, the cellular ontogeny of which has been
    precisely mapped, has 1,179 and 1,090 distinct somatic cells (including those that undergo
    programmed cell death) in the male and female, respectively, each with a defined history
    and fate. Therefore, if we take the developmental trajectories and cell position into account,
    C. elegans has 103 different cell identities, even if many of these cells are functionally similar.
    By this reasoning, although the number of different cell types in mammals is often
    considered to lie in the order of hundreds, it is actually in the order of 1012 if their positional
    identity and specific ontogeny are considered.Humans have an estimated 1014 cells, mostly
    positioned in precise ways and with precise organization, shape and function, in skeletal
    architecture,musculature and organ type,many of which (such as the nose) show inherited
    idiosyncrasies. Even if the actual number of cells with distinct identities is discounted by a
    factor of 100 (on the basis that 99% of the cells are simply clonal expansions of a particular
    cell type in a particular location or under particular conditions (for example, fat,muscle or
    immune cells)), there are still 10^12 positionally different cell types.

    a fact which he uses to argue

    Although it is widely believed that intronic RNA is non-functional (simply being degraded
    and recycled after excision by splicing), there is another equally, if not more, plausible
    possibility — that introns are genetically active and that intronic RNA feeds genetic
    information into the regulatory network of the cell11,12.

    ncRNAs: a parallel digital regulatory system.
    If the possibility is entertained that
    introns are functional (actively transmitting
    genetic information through RNA
    molecules), then an entirely different type
    of regulation becomes possible, with an
    entirely different set of logical extensions
    and interesting predictions.
    First, it would mean that the genetic
    operating system of complex eukaryotes is
    fundamentally different and much more
    sophisticated than that of simple prokaryotes.
    Eukaryotic genes would express two types of
    information in parallel — proteins and (to
    borrow a term from neurobiology) EFFERENCE
    RNA SIGNALS that can communicate with other
    genes or gene products independently of the
    biochemical function of the encoded protein
    in the host transcript11–13. This leads to the
    deeper prediction that the emergence of a true
    parallel processing system was, in all likelihood,
    fundamental to the evolution and
    development of complex organisms11,12.

  45. HT to Bradford at TelicThoughts for this gem by several authors
    http://www.plosgenetics.org/ar.....en.0030085

    During RNA splicing, sequences (introns) in a pre-mRNA are excised and discarded, and the remaining sequences (exons) are joined to form the mature RNA. Splicing is regulated not only by the binding of the basic splicing machinery to splice sites located at the exon–intron boundaries, but also by the combined effects of various other splicing factors that bind to a multitude of sequence elements located both in the exons as well as the flanking introns. Instances of alternative splicing, where usage of splice site(s) is incomplete or different between tissues, cell types, or lineages, can be created by the interaction of sequence elements and tissue, cell type, and stage-specific splicing factors. To better understand constitutive and alternative pre-mRNA splicing, the authors describe a comparative genomics approach, using available mammalian genomes, to systematically identify splicing regulatory elements located in the introns proximal to exons. A quarter of the elements were tested experimentally, and most of them altered splicing in human cells. The authors also showed that that the intronic elements are close to tissue-specific alternative exons and are more likely to be located in specific positions in the introns, suggestive of potential regulatory function. These elements are also frequently found in tissue-specific genes, suggesting a coupling between expression and alternative splicing of these genes. Finally, the authors propose a strategy using the elements to identify the binding sites of several splicing factors.

  46. Jonathan Wells weighs in:

    Fact Free Science of Matheson

  47. Arthur Hunt (#13):

    I have read the paper you quoted. It is very interesting, and rich of information.

    While I will certainly take some time to analyze it in detail, I would like to offer you a very simple methodological reflection, not about the paper itself, which I find intriguing and convincing, but about the inferences which you and others seem to derive from it.

    So, my point is very simple. The paper, even with many technical points which should be discussed, is trying to give a snapshot of the transcriptomes and, in some measure, of the AS events. But where? In two human cell lines, HEK 293T, which is a specific cell line originally derived from human embryonic kidney cells grown in tissue culture, and Ramos B cells, a human Burkitt’s lymphoma cell line.

    So my question is: why are you inferring that the number of AS events observed in tghese two cell lines, even if we accept it as accurate, should in any way represent the total number of AS functional events in all human cell types and cell states?

    The point with transcriptomes is obviously that they are specific to a cell type, and even to a cell state. The observed transcriptomes are significantly different between the two cell lines used in the above research, which are not even normal human cells. So, we can certainly presume that other cell types (and cell states) will have different transcriptomes (and different AS events).

    So, if the general question is how many introns actively take part in AS events in the whole set of human cells, of every type and in every state, you cannot certainly infer the answer form a single study which takes into consideration only two specific transcriptomes, of two cultured human cell lines, one of which hembryonal and the other one neoplastic.

    So, I stick to my statement that the available evidence is perfectly compatible with an important role of introns in AS (I will not quantify how many are implied, simply because we have no way to know for certain, at present).

    And that is only part of the picture, because AS is only one of the possible functions of introns.
    As you yourself say:

    As far as the functional vs. non-functional business, there is one key fact that IDists ignore in all of this. I refer, of course, to the fact that intronic RNA is made and then thrown away. We don’t call it “junk” because we don’t know if it does anything, we call it so because it is discarded.

    (OK, OK, so maybe we should be calling it “garbage DNA” instead of “junk DNA”.)

    As I learned on the 14th of May, and in many, many past discussions, the “garbage disposal” may be a central feature of the cell, required for all manner of molecular, physiological,and organismal function, but it is not on the IDists’ radar screen.

    I don’t agree with you. Why do you think that IDists are not aware that intronic RNA is made and then discarded? First of all, practically everything in the cell is “made and discarded”. Cells are typically “far from equilibrium” systems. Some structures are more stable, others more transient. But that’s no reason to infer that the transient ones are less functional. On the contrary, they could be transient exactly because that is connected to their function.

    IOW, while mRNA has to migrate into the cytoplasm and direct protein synthesis before it can be discarded, intranuclear RNA, which includes intron RNA, is probably implied in quick and subtle regulatory functions, its time of survival can be critically important to those regulation networks.

    There is indeed a lot of current research about the regulatory role of nuclear RNA, but I am sure that you know that better than I do.

    Finally, about terms like “junk”, or “garbage”, and so on, you should know that the concept of “junk” has been used for years by darwinists to imply that 96% of the human genome was non functional and represented an accumulation of evolutionary errors. That has been considered by many as an important argument in favour of the darwinian model of evolution.

    Indeed, terms like “junk” or “garbage” are simply not justified, and never were. The only appropriate term would be “non protein coding DNA”.

  48. Correction:

    The citation above stops at “I don’t agree with you.” The rest is mine.

  49. I got an novel idea Maya, Matheson, Hunt. Instead of dogmatically presupposing we are just a bunch of cobbled together junk, as only the most refined evolutionary thinkers are allowed to think, why don’t we allow for the completely absurd notion that we could just possibly be ,,,,

    Fearfully and Wonderfully Made – Glimpses At Development In The Womb – video
    http://www.metacafe.com/watch/4249713

    You are so beautiful – Joe Cocker
    http://www.youtube.com/watch?v=wlDmslyGmGI

  50. Not to put a fly in the ointment but the ID position in no way rest on the percentage of the non coding DNA that has function. It is certainly greater than zero and probably much less than 100%. The higher this percentage the stronger the ID case is but even if it is relatively low it does not make a dent in the ID argument.

    So argue all you want and make it interesting but everyone should keep in the back of their mind that the actual percentage may not affect the strength of the anti ID argument. If the percentage is fairly high then it is a very strong ID case and definitely weakens the anti ID position. If it is relatively low then it no way undermines the ID case nor weakens its position. ID can just not claim this particular point. What we have here is a desperate attempt to make sure the percentage is not high because that would be a devastating blow to the anti ID people. It may not be all that high and it will probably be years before we find out the truth.

    This is just a caution to the pro ID people. Do not go to the wall on this. The percentage could be fairly low and the complexity so overwhelming in the actual coding and regulatory parts that it boggles the mind that it could happen by chance. The remaining non functional DNA may be there as a result of an extremely functional process that is very complicated but well designed and which leaves excess DNA as a result.

  51. Jerry, Seeing as the most glaring mistakes in molecular biology have been made by people UNDERESTIMATING the complexity of the cell, I feel rather comfortable presupposing function for the “junk”, and I don’t mind “going to the wall”, as you put it, at all, for I have a strong feeling it will be the neo-Darwinists going to the wall for their beliefs, and indeed being buried by that wall when the wall comes crashing down on them. Shoot I am so bold as to predict any completely non-functional part of the genome that may be found will be the result of degradation, and certainly not the result of evolutionary processes just spinning through gazillions of sequences in DNA code trying to find a that elusive functional sequence:

    Stephen Meyer – Functional Proteins And Information For Body Plans – video
    http://www.metacafe.com/watch/4050681

    Evolution Vs. Functional Proteins – Where Did The Information Come From? – Doug Axe – Stephen Meyer – video
    http://www.metacafe.com/watch/4018222

  52. (30) veilsofmaya:

    @uoflcard

    You wrote:

    i.e., argument from ignorance.
    </blockquote:But then wrote:

    I’m still waiting for the evidence or model that makes it remotely reasonable to expect law and chance, devoid of intelligence, to create functional, complex, specified information, at least within the probabilistic resources of the history of the known Universe.

    Should I assume you’re just as open to the idea that the possible “functions” of non-coding DNA could resolve many if not all of the supposedly insurmountable problems you’ve just mentioned?

    Not exactly sure what you’re implying here. First of all, I’m open to any idea. But the idea that non-coding DNA is possibly the source of the rest of the information in the genome just moves the goal posts. Where did THAT information come from? If it really is an amazingly complex algorithm capable of sculpting life, and it operates purely by law and chance (i.e. naturally), then it must contain more information than it creates. So where did that fCSI come from?

    Arguing that law and chance probably did not create the information of life is not an argument from ignorance (if that is what you were trying to somehow imply) anymore than arguing that the “flying spaghetti monster” doesn’t exist is an argument from ignorance. We are not omnipotent, therefore we will always be ignorant, to some extent. So we choose which currently available explanation explains our observations most accurately. Right now there is nothing beyond extreme faith, or even the need for naturalism to be true, to believe that law and chance made all of the complex funcitons of life, including human consciousness. But we have another possible explanation for fCSI, one we observe and experience on a daily basis: Intelligence.

    This is vastly different than someone denying the possible funciton of an string of non-coding DNA. We are discovering new function of non-coding DNA on a weekly basis, it seems. It therefore seems naive (indeed, a true argument from ignorance) to deny function to any genetic string that has not been extensively studied.

  53. We observed 95% of the splicing events expected in this data set, given the current sequencing depth (Table 1) (16). We identified 4096 previously unknown splice junctions in 3106 genes, mostly called by single reads and unique to one cell type (Table 1). Many of these junctions were associated with actively transcribed genes exhibiting more exons than average, pointing to rare splicing events. Approximately 6% of all splice-junction reads identified AS events (6416 junctions in 3916 genes HEK and 5195 junctions in 3262 genes in B cells) (table S9).

    Art,

    How can you say introns are involved in only 6% of the Alternative splice events.

    This paper says only 6% of the READS are alternative splice events, it says nothing of the amount of introns involved in those 6% of the reads that are AS events.

    Please clarify for our readers.

  54. Art,

    You can’t argue that a particular gene in an already differentiated cell implies the gene is limited to only 6% alternative splicing! You have to look at every cell that contains that gene!!!!! See Mattick’s tally of the number of differentiated cells. You’re basing your claims on 1 cell, whereas we might have to examine 10^12 positionally different cell types to make an exhaustive search.

    But based on diffentiation alone, it would seem that the facts accord better with Sternberg and Wells.

    I welcome hearing from you. Thanks for visiting.

    Sal

  55. For the reader, I’m claiming Art is making an incorret, non-sequitur inference from the literature he is citing (Sultan’s paper).

    You can’t claim that introns are only limited to be involved in only 6% of alternative splice events. The 6% figure only references the number of reads that are alternative splice events, it says nothing of proportion of Alternative splice events that involve introns. I consider this a technical mistake.

    We have in this particular case:
    6% of reads are Alternatively Spliced

    Now take all those Alternative Spice events, what proportion of them involve introns? It is possible 100% could involve introns. You certainly can say since 6% of the READS are alternatively splice that therefore 6% of alternative spices involve introns. Such a conclusion does not logically follow from the premise, but constitutes a mis-reading of the literature.

    Art is welcome to defend his claim and correct mine (if I’m wrong). Thanks in advance Art.

  56. Let me use a more everday example to clarify what I think Art’s misreading is.

    The mistake is like saying:

    6% of cars have GPS built in, therefore only 6% of cars with built-in GPS have a with built-in GPS have a GPS signal processor in their GPS system

    the correct characterization is

    6% of cars have GPS built in, but 100% of cars with built-in GPS have a GPS signal processor in their GPS system

    Of course, in the case of introns we don’t know for sure if 100% of all Alternative Splice events involve introns, but I’m claiming you can’t make the inference that only 6% of all Alternatively Spliced events involve introns from Sultan’s paper.

    I’m inviting Art to clarify, and I thank him for participating in this scientific exploration.

    Sal

  57. Sal, lightly skimming for articles on Introns, I found this:

    Introns — Nonsense DNA –
    Excerpt: And surprisingly, the vast majority of intron DNA sequences the scientists examined were of unknown origin.,,, Almost all of the introns the IU Bloomington biologists located possessed a sequence of indeterminate origin. Only one of the 24 identified sequences bore a resemblance to a specific DNA sequences associated either with the Daphnia genome or its parasites. The other 23 introns had sequences that appear to have been improvised by the machinery responsible for DNA synthesis. “Our molecular analyses have enabled us to reject a number of hypotheses for the mechanism of intron origins, while clearly indicating an entirely unexpected pathway — emergence as accidents arising during the repair of double-strand breaks,” Lynch said.
    http://www.sciencedaily.com/re.....111148.htm

    You Know Sal, I think I am really beginning to love these intron sequences 8)

  58. ART asks:

    Are we all in agreement with Sternberg and Wells when they claim that every intron in every human gene whose RNAs are subject to alternative splicing are themselves alternatively spliced?

    They did not make that claim, that is your mischaracterization.

    Also you have to make a distinction between the specific gene behavior in a specific cell type versus the collective behavior of the gene in all cell types where the gene exists.

    I’m afraid your EQUIVOCATING the behavior alternative splicing in one specific cell type when Wells is cleary discussing the collective involvement of introns in all cell types in the manner Mattick discusses them.

    By the way, Wells also references Sultan’s papers.

  59. @scordova (#42)

    It seems you analyzing Matheson’s quote without using any context at all. If that’s the case then, yes, it’s impossible to say that anything couldn’t have some vague function in some form or another at some point in time or some scenario.

    However, Mathasion clearly provided context when he use the phrase known to have “important functional roles.” Note the qualifiers “know to have” and “important functional roles”.

    Removing these objections, it seems the real issue is that your merely offended by the idea for reasons that are theological in nature.

  60. V,

    However, Mathasion clearly provided context when he use the phrase known to have “important functional roles.” Note the qualifiers “know to have” and “important functional roles”.

    NOT KNOWING IF AN INTRON HAS FUNCTION DOESN’T MEAN THE INTRON HAS NO FUNCTION! GET A CLUE!

  61. Spare Tires and Operating Systems:

    I should point out there are legitimate and illigitimate ways of characterizing functions.

    It would be illegitimate to cherry pick all the days where spare tires on cars are not used. It would be illegitimate to say, “the spare tire wasn’t used on July 19, 2001, therefore the spare tire serves no function”.

    In similar fashion, it would be illigitimate to say certain features of an operating system (like Windows 7) aren’t functional merely because we find computer users who don’t use all the features of the operating system!

    We certainly might find introns in some cells that are not used, but it would be deeply improper to generalize the behavior of introns in one cell type to all cell types. In fact Mattick argues introns are used differently in each cell type.

    If indeed the cell uses operating systems like modern computers, and if cells have backup systems like spare tires, we would actually expect cells to have functional capabilities that are not always utilized. The lack of utilization 100% of the time is not evidence against function anymore than the lack of use of a spare tire or unused feature of an operating system is evidence against its function.

  62. The reason I mentioned spare tires and operating systems is that Art is referencing the behavior of a single cell type to make his case.

    There are, according to Mattick,
    10^12 or 1,000,000,000,000 positionally differentiated cell types. I’d say even if Art makes a case for one cell type, (and I’m still disputing he got the account correct), he is making an awfully hasty generalization given we have, according to mattick 1,000,000,000,000 positionally differentiated cell types. :-)

    It would illegitimate to say that because you found a computer user that only uses 5% of Windows 7, therefore 95% of Windows 7 is non-functional!

    I claim Art’s citation of from Sultan’s paper is equally flawed. He is more than welcome to contest my characterization of what he said.

    Thanks in advance to Art for his response.

  63. There is also a possible Equivocation in the way Art is arguing against Sternbergs claim:

    At least ninety percent of gene transcripts undergo alternative splicing, and there are at least 190,000 introns in the human genome.

    A charitable reading is 90% of the KINDS of transcripts existing emerged from alternative splicing.

    How can this be? a manufacturing analogy is inorder.

    Say we have 1000 cars, 900 of them are identical, but 100 of them are unique, and the unique cars emerged out of Alternative Manufacturing (Splicing if you will). Thus we have 101 different kinds of cars, and 100/101 = 99% emerged via Alternative Splicing.

    Thus even though 90% of the physical cars did not go through alternative splicing, 99% of the kinds of cars went through alternative splicing (so to speak).

    Hopefully the clarifies further the mis-use by Art of Sultan’s paper. :-)

  64. So, for further clarity, I would like to formulate again the main question I formulated in my #47 to Arthur Humt about his interpretation of the Sultan paper, and which, I believe, has been restated in a slightly different way by scordova:

    Even if it were true that only 6% of the introns (indeed, of the reads) were involved in AS in the Sultan study, that is in two specific human cell lines, why should that mean that the other introns, all or most or many or some of them, are not involved in AS events in other human cell types and cell states?

    Different cell types are defined by different transcriptomes. That means different genes involved, and very likely different AS events. It’s perfectly reasonable to assume that, if 6% of introns are involved in AS in just two cell types, a greater number, probably a much greater number, will be involved in all possible AS events in the total set of human cell types.

  65. Sal, no matter how you try, you cannot twist Sternberg’s and Wells’ words to mean anything other than that they believe all introns (at least all introns in genes subject to alternative splicing) are themselves alternatively spliced.

    Heck, the unspoken consensus here seems to be in agreement with this. That is why there is so much effort to argue that, in fact, all introns do undergo alternative splicing.

    The suggestion that perhaps different sets of introns are subject to differential splicing in different cells or tissues is a good one. But there is nary an iota of evidence to suggest that the scale of such events even comes close to rescuing Sternberg and Wells from their gaffe. Some studies suggest a very modest scope of such events. IIRC (the paper is on another computer), the much-lauded “splicing code” paper used for confirmation studies an exhaustive set of some 11,000 or so alternatively-spliced exons (the much better unit to be talking about, reflecting yet another blunder on the parts of Sternberg and Wells, but that’s another story altogether) that came from an analysis of many, many more than two cell types. OTOH, I am aware of no data – not a single study – that would support the suggestion that each and every intron may be subject to functionally-significant alternative splicing in at least one cell type. (Remember, were talking about a claim that there are more than 150,000 AS introns.) So, while the suggestion is fanciful and may be true to a rather limited extent, it hasn’t the support of data to rescue Sternberg and Wells.

    There’s one more bit of irony I haven’t yet mentioned. The bigger picture here is the need by IDists to find function for the 1 billion + bp of intron-encoding DNA. Recalling again the “splicing code” paper (as well as one of the links I give), all of the intronic cis-elements involved in AS take up all of 600 nts (or less) of your generic AS intron. If each and every intron has 600 nts of such cis elements, that adds up to less than 2% of all intronic sequence. In other words, none of these considerations even makes a dent in the “junk DNA” problem.

    (I can see some confusion about the Sultan paper regarding what the authors mean by reads and sites. If this posting finds the light of day before Wed, I may add another one to explain things better,so readers are less confused by things.)

  66. That should be 20% in second to last paragraph, not 2%. Sorry about that, and any other typos that sneaked through. I’m especially having problems with my space bar, and it makes for rather interesting “words”.

  67. gpuccio:

    So, for further clarity, I would like to formulate again the main question I formulated in my #47 to Arthur Humt about his interpretation of the Sultan paper, and which, I believe, has been restated in a slightly different way by scordova:

    Even if it were true that only 6% of the introns (indeed, of the reads) were involved in AS in the Sultan study, that is in two specific human cell lines, why should that mean that the other introns, all or most or many or some of them, are not involved in AS events in other human cell types and cell states?

    EXACTLY!

    And the number of AS events which Sternberg discusses does not refer to the number of physical transcripts that emerge from the AS events but rather the number of varieties of transcripts.

    That is why I made the following distinction:

    A charitable reading is 90% of the KINDS of transcripts existing emerged from alternative splicing.

    How can this be? a manufacturing analogy is inorder.

    Say we have 1000 cars, 900 of them are identical, but 100 of them are unique, and the unique cars emerged out of Alternative Manufacturing (Splicing if you will). Thus we have 101 different kinds of cars, and 100/101 = 99% emerged via Alternative Splicing.

    Thus even though 90% of the physical cars did not go through alternative splicing, 99% of the kinds of cars went through alternative splicing (so to speak).

    And thus this invalidates the line of argumentation that focuses on a single cell type. The issue must make an estimate that includes the approximately 1,000,000,000,000 cell “types”.

    Wells performed the method of estimation. We can clearly see Wells was not referring to sheer number of physical transcripts generated, but the number of different kinds of transcripts.

    Here is a rough calculation.

    Wells points out:

    scientists reported that the majority of human genes generate almost eight different messenger RNAs.

    Worst case 50% of genes have 8 different mRNA’s. That means on worst case, on average each gene has 4 different mRNA, which implies, worst case 3 out of 4 alternative splices, or 75%.

    You can’t just take one cell type and say, look, that gene had no alternative splices! That like picking a day a spare tire is not used and then saying, “see spare tires serve no purpose since on that day it wasn’t used” or “the lexmark printer driver on Windows 7 serves no purpose because we saw Windows 7 users that didn’t use that printer driver”.

    I claim that Art is mis-using Sultan’s paper in a similar way to make his point.

    I appreciate his participation here, but I think his line of reasoning is flawed.

    Finally, I should mention, it is perfectly reasonable that a cell has many unused or underutilized features. It doesn’t make the features functionless any more than the unused features of Windows 7 among various Windows 7 users.

    It actually is good design practice to make generic capabilities that are not too customized. This allows easy maintenance and manufacture. The trade-off is that you have a lot of unused duplication. But we see from modern experience with operating systems, large amounts of unused function is the norm. We have little reason to say features of cell architecture won’t have the same design features! In fact it is more consistent with the modern practice of complex systems engineering, particularly information intensive systems.

    Software engineers in particular will appreciate this fine point that seems to elude Darwinist biologists.

  68. Dr Hunt,

    Yes, I agree with you. It seems that Dr Sternberg thinks that each of the 7.6 introns per gene is involved in alternative splicing, rather than at least one out of the 7.6 introns, which is all that is implied by data. If each of the 7.6 introns was involved, then each gene would code for over 250 different proteins.

  69. scordova,

    If you approve of Mattick’s speculations, do you also agree with his assumptions of life beginning 4.2 billion years ago, common descent, and the Cambrian explosion as a natural event?

    Not that I agree that there is a positional cell type, but if positional data needed to be encoded in RNA, you could code for 10^12 positions in 20 nucleotides.

    20. And the rest would still be junk.

    An interesting test of Mattick’s ideas would be to see if there is any correlation between trancript complexity and weight. According to him, fat people need more complex RNA – so many more positions!

  70. It actually is good design practice to make generic capabilities that are not too customized. This allows easy maintenance and manufacture.

    Nothing like unrelated functions linked together, like hair color and texture, and tameness.

    Makes code maintenance a snap.

    When I worked as a programmer, I was required to make my code as cryptic and entangled as possible. I’d have been fired if I wrote something that the guy following me could understand and maintain without fear of breaking several unrelated functions.

  71. off-topic, but has anyone done a substantial response to this at PT

    http://pandasthumb.org/archive......html#more

  72. One observation and one question:

    Observation: It seems that Art Hunt and veilsofmaya come here to contest Sternberg and all they really have are rhetorical devices. (I am especially disappointed, but not entirely surprised, that gpuccio has discovered that the paper Art Hunt cites deals with almost esoteric cell lines—this is almost a kind of duplicity)

    Question (for both Art and veils):

    Tell me, which is more highly converved, the coding, or the non-coding, portions of DNA? (Would you like to talk about this?)

  73. off topic Phaedros: the retina was addressed here recently by David Tyler:

    The contribution of glial cells to human vision acuity
    http://www.arn.org/blogs/index.....s_to_human

    and here:

    The vertebrate eye does not have a compromised design
    http://www.arn.org/blogs/index.....ve_a_compr

    and here:

    http://www.uncommondescent.com.....on-acuity/

    From looking over the PT article it is obviously “damage control” for a very embarrassing development.

  74. Sometimes it seems incredibly difficult to reconcile or even attempt to synthesize these two outlooks on the evidence. It’s like you have two extreme opposites, one where the glass is half full and one where the glass is half empty and there’s no intermixing between the two.

  75. By the way, is everyone off debating on a different blog?

  76. Phaedros,

    Not that I’m aware of except maybe for Dr. Hunter’s blog.

    I posted some of my comments on Larry Moran’s blog, this is how he responded to me:

    Unfortunately for you, the human genome wasn’t designed by an engineer, unless it was the same one who works for BP.

    My response: so it’s perefectly fine for Darwinists to apply their supposed design standards in evaluating systems (i.e. they label thinks junk at their own whim), but when I cite common engineering practice, somehow that’s not a valid benchmark?

    There you have it from one of the trio.

    As far as PT goes, Art is one of the authors there. He would be the most able to respond, but as I said, I think he is mistaken. He’s attacking arguments that Sternberg and Wells aren’t making, imho.

    I will leave it to Art however to have his say regarding the objections several of us have put forward at UD.

  77. Nothing like unrelated functions linked together, like hair color and texture, and tameness.

    Makes code maintenance a snap.

    When I worked as a programmer, I was required to make my code as cryptic and entangled as possible. I’d have been fired if I wrote something that the guy following me could understand and maintain without fear of breaking several unrelated functions.

    That misconstrues what I said.

    I point to the readers to a common engineering practice of constructing classes that contain more instructions than the immediate need of the caller. That is the case of with overloaded methods in Java

    Overloaded Method

    There are probably hundreds of software subroutines in the operating system on your workstation that are not being used. Are you going to argue since these components aren’t being used by you that they have no design for a function?

  78. Thank you Art for responding.

    The suggestion that perhaps different sets of introns are subject to differential splicing in different cells or tissues is a good one.

    Thank you for acknowledging this.

    Art wrote:

    Sal, no matter how you try, you cannot twist Sternberg’s and Wells’ words to mean anything other than that they believe all introns (at least all introns in genes subject to alternative splicing) are themselves alternatively spliced.

    Then please provide the specific quote from the readers where they say:

    all introns (at least all introns in genes subject to alternative splicing) are themselves alternatively spliced

    Further you said:

    . That is why there is so much effort to argue that, in fact, all introns do undergo alternative splicing.

    Who makes that argument? Not Sternberg, not Wells. Sternberg concedes the possibility that not all introns are involved in splicing:

    Even if we were off by a factor of two, we would still be left with 85,500 introns that function in the process of alternative splicing.

    and Wells wrote:

    Since each splice requires two junctions, and humans probably have between 20,000 and 25,000 genes, this suggests an average of 2 introns per gene involved in alternative splicing. In 2009, scientists reported that the majority of human genes generate almost eight different messenger RNAs. But in order for a gene to generate eight alternatively spliced messenger RNAs it must contain at least three protein-coding segments, and thus at least two introns.

    So the published scientific evidence indicates that alternatively spliced genes contain at least two introns—not the one intron assumed by Moran. This would yield a lower figure than Sternberg’s original estimate—45,000, to be exact—but this is still a lot more than 1,000.

    Such claims seem hardly consistent with your characterization that they insist “all introns are involved in alternative splicing”.

    At least to your credit you’re not repeating Mathesons gaffe where he argues if we don’t know at this time an intron has function, then it therefore doesn’t have a function.

    You don’t have to agree with Wells and Sternberg’s estimate. You may argue you are not aware of various studies that would make you agree with Wells and Sternbergs estimates.

    But that is not the same thing as saying we know for sure introns have no function (as Matheson asserts).

  79. What Sternberg actually said:

    http://www.evolutionnews.org/2.....35381.html

    Therefore, 22,500 genes x 7.6 introns/gene = 171,000 introns involved in alternative splicing.

    This is just a rough estimate, of course. And as I wrote in my original critique of Matheson, even if I’m off by a factor of two we are still left with far more functional introns than Matheson acknowledges. This compels me to ask Steve Matheson: How exactly did you come up with your estimates? And what about you, Larry Moran? What sort of arithmetic are you using?

    In any case, I don’t know how this can be characterized (as Art claims) to:

    they believe all introns (at least all introns in genes subject to alternative splicing) are themselves alternatively spliced

    Holding out the possiblity of being off by a factor of 2 hardly constitutes belief that ALL introns are involved in alternative splicing.

    Finally, Wells gave a pretty good alternative estimate. Any objections to Well’s line of reasoning?

  80. In his ENV piece, Wells said:

    In his ENV piece, Wells states:

    Yet Hunt cited no scientific literature, just as Moran cited none to support his assumption that only one intron per gene may be involved in alternative splicing.

    Actually, a 2008 article in Science reported 94,241 splice junctions in human messenger RNAs. Since each splice requires two junctions, and humans probably have between 20,000 and 25,000 genes, this suggests an average of 2 introns per gene involved in alternative splicing.

    Wells’ math “adds up” only if 94,241 is the number of junctions in alternatively-spliced introns, no?

  81. Seeing that alternative (gene) splicing requires knowledge- what to splice, how to splice and when to splice it- how can anyone with knowledge of alternative (gene) splicing still be on the side of the blind watchmaker?

  82. Wells’ math “adds up” only if 94,241 is the number of junctions in alternatively-spliced introns, no?

    No, because there is also another line of evidence he cited.

    Wells writes:

    scientists reported that the majority of human genes generate almost eight different messenger RNAs.

    My take is worst case 50% of genes have 8 different mRNA’s. That means on worst case, on average each gene has 4 different mRNA, which implies, worst case 3 out of 4 splices are alternative splices, or 75%.

    So we have 20,000 genes that generate 80,000 transcripts, 60,000 of which are emerge from alternatively splicing, and we have 2 introns for each splice, that’s about 120,000. Of course, I suppose it’s conceiveable we have the same intron involved in two separate alternative splicings, so instead of 2 introns, we could say maybe 1.5 introns per AS, so that’s 90,000 introns involved in AS.

    As Wells points out, this is a lower bound estimate.

    Thank you again for your criticism. I’m sure the readers find it substantially more astute and well reasoned than Mathesons gaffes.

    The Barash paper in May 2010 published in Nature also suggests that introns are integral to the read/write architecture and decoding process.

    Matheson is dismissive of regions that may even function as spacers (not that I’m sayin introns are only spacers). To which I respond,

    many DvD’s and CD’s frequently have unused, blank regions. Will matheson suggest we could just physicallly remove those regions and expect a CD or DvD to function. Is it a good argument that the blank regions have no function, that have no design, or that it constitutes un-intelligent architecture?

    Or how about the blank spaces in bar codes, do they serve function or not. :-)

    To your credit Art, you don’t seem to suffer from Mathesonian illogic as much as Matheson. You strike me as far more learned and astute.

  83. Art wrote:

    As I learned on the 14th of May, and in many, many past discussions, the “garbage disposal” may be a central feature of the cell, required for all manner of molecular, physiological,and organismal function, but it is not on the IDists’ radar screen.

    Are you suggesting this would be a good area of investigation for ID proponents? If so, thank you for the tip.

    Sal

  84. By the way, Matheson is having a bit of a meltdown:

    In Matheson’s Sour Grapes Whining

    “3. Your Discovery Institute is a horrific mistake, an epic intellectual tragedy that is degrading the minds of those who consume its products and bringing dishonor to you and to the church. It is for good reason that Casey Luskin is held in such extreme contempt by your movement’s critics, and there’s something truly sick about the pattern of attacks that your operatives launched in the weeks after the Biola event. It’s clear that you have a cadre of attack dogs that do this work for you, and some of them seem unconstrained by standards of integrity. I can’t state this strongly enough: the Discovery Institute is a dangerous cancer on the Christian intellect, both because of its unyielding commitment to dishonesty and because of its creepy mission to undermine science itself. I’d like to see you do better, but I have no such hope for your institute. It needs to be destroyed, and I will do what I can to bring that about.”

    Sounds like someone expressing sour grapes after being discredited. :-)

    Steve needs to get spooled up on the latest literature. He could start with the paper in the Prestigious Scientific Journal Nature published May 2010:

    http://www.ncbi.nlm.nih.gov/pubmed/20445623

    And it begins by saying:

    “Transcripts from approximately 95% of multi-exon human genes are spliced in more than one way.

  85. Sal,

    Foresight and planning.

    IOW not every possible splicing combination has been required.

    The introns not involved in splicing now are (could be) for future use if required- TBD.

  86. 86

    Matheson: “This past week I was at a remarkable conference run by the BioLogos people, in Massachusetts near where I used to work as a postdoc. It was so refreshing to be with serious Christians who are serious about science and truth-telling.

    That was poor. Matheson can’t defend his argument, and at the same time can’t mount a deliberate distinction between discussing someone’s evidence and questioning their faith.

    So go for broke and drag Jesus into it.

    Great.

  87. Was Matheson once banned from this site? Or does he simply avoid meanaingful dialogue? The last time he was here, he left just when things started getting interesting and I never knew why. Was it our choice or his?

    If it is the former, why not rescind the order and allow to make his unpersuasive case right here so we can refute it?

  88. So, I take it my comments are deleted without any reference to their removal?

  89. So, I take it my comments are deleted without any reference to their removal?

    Yes. Thank you for your participation, other discussions at UD might be better suited for your comments, but not this thread.

    Your comment was initially put in the spam buffer by me since they repeated illogical arguments that had already been taken care of.

    When the comment reappered I deleted it.

    At this time you are still free to discuss on other threads and you can offer technical data here. Beyond that, if I find that you’re repeating erroneous points that have already been refuted, as a service to readers, such comments will be edited out.

    Thank you however for your submissions.

  90. Was Matheson once banned from this site? Or does he simply avoid meanaingful dialogue? The last time he was here, he left just when things started getting interesting and I never knew why. Was it our choice or his?

    If it is the former, why not rescind the order and allow to make his unpersuasive case right here so we can refute it?

    Good idea. I have no access to the banned list. Clive or Barry might have to get involved on that one.

    I’d like to express my thanks to Dr. Arthur Hunt for participating here.

    As far as I know, Larry Moran was banned by Dave Scott, however, let me provide this Observation by Jonathan Wells regarding Moran:

    And Moran’s guess that only about 5% of human genes undergo alternative splicing is flatly contradicted by 2008 articles in Nature and Nature Genetics, as well as the 2010 Nature article cited by Sternberg. In lieu of factual support for his claim, Moran ridiculed Sternberg for giving “no indication that he understands the controversy” and basing “his entire fairy tale on a value [i.e., 95%] that has been pretty much discredited.”

    Yet Moran provided no justification for his ex cathedra pronouncement that the 95% figure has been discredited. He simply brushed aside the 2008 and 2010 articles in Nature and Nature Genetics and their eighteen co-authors—nine of whom listed their affiliation as Moran’s own institution, the University of Toronto.

  91. Matheson allows comments at his blog, Quintessence of Dust.

  92. gpuccio @ #47:

    Sorry for losing this in the flurry.

    You said, when I mentioned how the “garbage disposal” isn’t on the radar screens of IDists:

    I don’t agree with you. Why do you think that IDists are not aware that intronic RNA is made and then discarded? First of all, practically everything in the cell is “made and discarded”. Cells are typically “far from equilibrium” systems. Some structures are more stable, others more transient. But that’s no reason to infer that the transient ones are less functional. On the contrary, they could be transient exactly because that is connected to their function.

    Yes! (To everything but the first sentence.) But the fact of the matter is that IDists either don’t appreciate or are opposed to these concepts.

    As an example to support my case, allow me to summarize my experience at Biola on May 14. I approached this as a chance to grill the leader of the ID movement, the person who has written the defining book on the subject, one who states often in the book that his research, as it were, makes him well-appointed to pass judgment on the science of design and anti-Darwinism.

    I only got to ask a few questions, but two of them touched on the theme of the “garbage disposal”. I asked Meyer about polyadenylation,and included in a listing of its importance the fact that it is important for RNA degradation (in bacteria, and for the degradation of the numerous nuclear junk RNAs that Sternberg is vainly trying assign function). Meyer actually did not seem to even know what polyadenylation is (I had to repeat the term, and I feared I would have to spell it out), and he declined to challenge my assertion that junk RNA really is junk. In other words, the crucial role that RNA degradation plays in regulation and quality control was just not on his radar screen.

    Neither was the entire field of E3 ubiquitin ligase-mediated degradation of proteins, and the central importance of the process in biology. When I mentioned this subject, he seemed totally perplexed. And he actually agreed with my argument, made using this example, that the analogy between machines and living cells was not a good one. So, again, the leading light of the ID movement was totally unaware of a crucial process, one that involves degradation, turnover, and “garbage”.

    So, on top of years of making similar points on the ARN and ISCID boards, (and here, when Dave Scot told me that this approach to regulation made no sense), this most recent experience reinforces my claim. I think it’s valid, and it reflects the disconnect between the ways cells really work and the ways that “design principles” might work.

  93. 93

    Art,

    Certainly it is appreciated that you are contributing here, not withstanding your self-serving and unnecessary personal attacks against Meyer.

    I haven’t had the opportunity to listen through the audio of the debate, yet I wonder. Perhaps what you perceived at being perplexed in Meyer, was a misread on your part. Perhaps it was more aligned with him being underwhelmed – if not dismayed.

    The role of degradation as a mechanism in regulation does absolutely nothing to the core of his argument – which is (I am certain) what he was there to defend.

    If you want to make the argument that the source of functional complexity/information can be found within the question of junk DNA, then just make it.

  94. Arthur Hunt (#92):

    First of all, I want to thank you for your intellectually honest and deeply competent contribution to this debate. That is really from the heart, there is nothing I appreciate more than good interlocutors, especially those which have different ideas.

    That said, I must say that I agree with your last post completely on the scientific points, with some distinctions on a couple of points:

    1) I find nothing strange if Meyer was not specially sensitive to the points you raised. ID is a work in progress, nobody knows all, and nobody represents ID on a plane of authority. As all scientific paradigms, ID is of all and for all. People like Behe, Dembski and Meyer, IMO, deserve a very deep repsect and admiration for the work they are doing, and have contributed immensely to the cause of ID, but nobody of them is a dogma or an absolute authority. One of the problems in ID is the paucity of biologists in the group (which can easily be explained in many ways, not necessarily those that darwinist would like to argue :) ). That’s why the contribution of serious darwinist biologists to the ID debate can really be precious. As far

  95. Arthur Hunt (#92): (continuation: the previous posy gor posted almost by itself while I was writing it :) )

    So, as I was saying, as far as I can see form your own words, Meyer himself was not in principle unreceptive to your suggestions, and that’s a sing of open mind and humbleness, which are the greatest virtues in scientific debate.

    Anyway, it’s not my duty to defend Meyer. I suppose he can do that himself perfectly well. So, let’s go to the second point, which is certainly more important.

    2) While I perfectly agree with you about the supreme importance of all degradation mechanisms in biological regulation (there are lots of examples, including obviously those you cited, which are of utmost relevance), I must say that I don’t understand the concepts which you seem to derive from that fact. You say:

    So, again, the leading light of the ID movement was totally unaware of a crucial process, one that involves degradation, turnover, and “garbage”.

    and:

    So, on top of years of making similar points on the ARN and ISCID boards, (and here, when Dave Scot told me that this approach to regulation made no sense), this most recent experience reinforces my claim. I think it’s valid, and it reflects the disconnect between the ways cells really work and the ways that “design principles” might work.

    First of all, just as a humourous note, I would mention that you were not the only one who had some problem with DaveScot: many of us, including me, share that experience :) With this, I don’t want in any way to criticize him, or diminish his contribution to this blog, but just state a well known fact.

    But let’s go to the substantial point. Leaving apart the reference to Meyer, I believe what you are saying is: the way cells work is different form the way machines work; so, while machines obey to design principles, cells don’t (more or less, I just want to make the point more explicit here, it’s not my intention to put words in your mouth…)

    If that is your point, then I don’t agree. There is no doubt that cells work in a different way, let’s say, than an automobile or a computer. They are different kinds of machines, but still machines they are. And still designed they are. Obviously, the implementation of design is different in different kinds of machines: The design of a mechanical engine is not the same as the design of a software program, or of a radio transmitter. Each situation needs specific approaches, The same nature of the chosen hardware material poses rules and constraints to the design. But why do you think that such a difference implies a difference in the “principles” of design? The only universal principle of design is that the designer, a consciuous intelligent being, is responsible for searching and finding some ordered structure which can accomplish a specific function. That process, well known to programmers, is called implementation, and it is universally valid for all designed things, however big the differences in the implementation procedures may be.

    Moreover, It’s not true that the importance of degradation and turnover of functional units (I still don’t see why you use the term “garbage”) is unique to biological machines. Whoever has some acquaintance with programming, knows well that, especially in object oriented programming, the building, span of life, visibility and degradation os softwrae objects is one of the leading principles for the programmer. Objects are continuosly built and destroyed in software programs, so that they may perform their function and then release the necessary resources. Errors in these finely regulated networks can really affect the working of the program.

    So, again, where is the difference?

    IMO, the finely regulated network of synthesis, modifications and degradation which we can see in all biological networks, but especially in protein networks and in the extremely complex and crucial nuclear network of transcription factors and regulatory RNA elements, which we are just beginning to understand, are and will increasingly become the best evidence of design in the cell.

  96. scordova,

    You’ve asked me to shift my discussion of introns to this thread, from your other Matheson thread.

    In your response there, you mention your airplane magneto example. I’m sure that if some set of introns is functional but redundant, knockouts would eventually reveal that fact. We know that magneto A is redundant with magneto B, not door handle F. Experiment would similarly reveal these details redundant function if they exist.

    You also raise the issue of function in context. I agree it is possible for knockouts to eliminate function that is not immediately obvious. The ultimate context in which function should be judged is competition against wild type mice in a wild environment. Again, this is a matter for the experimental design to include, not a reason to avoid doing the experiment.

    Knockout experiments have been very helpful in finding which specific sequences have which specific functions. If introns have function, knockouts can help elucidate that function. You have a testable prediction, why not use the tool?

  97. all of the intronic cis-elements involved in AS take up all of 600 nts (or less) of your generic AS intron. If each and every intron has 600 nts of such cis elements, that adds up to less than 2% of all intronic sequence.

    The only reason they looked at only 300nt (and not more) is because the more sequence you look at, the less likely you are to find bona fide features, because you lose statistical precision.

  98. The only reason they looked at only 300nt (and not more) is because the more sequence you look at, the less likely you are to find bona fide features, because you lose statistical precision.

    No, the reason for the 300 nt focus is because this is where the known intronic splicing enhancers/silencers lie. This region was determined by decades of biochemistry.

  99. That is simply not true, and is not supported by anything written in the paper.

  100. The ultimate context in which function should be judged is competition against wild type mice in a wild environment.

    Not necessarily. Consider blind cave fish. Their blindness is hypothesized by many (including myself) to confer advantage since it has lower metabolic load on fish in dark underwater caves (where seeing isn’t any benefit anyway). In such an environment, blindness confers advantage over seeing.

    Using the competition benchmark in the wild, do we then say the ability to see is junk? No!

    The way to elucidate function is not by selective advantage. Andreas Wagner and Lewontin have put forward arguments as to why, especially since fitness is difficult to universally define.

    Function is better elucidated via comparing architectures and pattern recognition. If an engineer is trying to understand how something works (like say a bridge or space ship), knocking parts out might be one way to make a detection, but it’s kind of clumsy!

    One technique to detect function is to take a given cell type and try to find ways to stimulate an alternative splice. This is not to different from techniques used in reverse engineering and it is less clumsier than knockout!

    An experimental example? Hmm:

    Corticotropin-releasing hormone triggers differentiation in HaCaT keratinocytes

    I’d say knockout should be a bit of a last resort, and should be done with the caveats I stated in mind.

  101. scordova,

    In the case of your example the function is not sight, but the appropriate suppression of sight. I think that would qualify as function if you found it in an intron.

    Clumsy? No need to be perjorative. Megabase knockouts are simply working on larger chunks of the genome to target the important areas for more detailed study later.

    Looking again at the reports on the megabase deletion experiments that have been done, it seems that the scientist are aware of, and sensitive to, your concerns. I’m sure if the DI conducted similar experiments, they would also be sensitive to them. The overall point from the perspective of our discussion is that it is a very powerful form of argument (to prove your point) to assume the negative and then reason to a contradiction. Doing megabase knockouts would be a fast way of doing that.

    BTW, here is an article I came across on function in gene deserts that is generally supportive of the idea of function in non-coding DNA. It may also provide some clues, methods, or possible collaborators for DI-funded experiments on this topic.

  102. Unfortunately for you, the human genome wasn’t designed by an engineer, unless it was the same one who works for BP.

    The problem with bon mots in technical debates is that they usually only reveal ignorance.

    The Deepwater Horizon disaster wasn’t the fault of BP engineers who issued warnings about the practices in place but with the corporate management and political regulators (yes this means Obama) who made decisions apparently based on hubris and greed.

    What’s illustrative of the “human genome wasn’t designed by an engineer” dig is that it is designed to dismiss not enlighten and very well be motived by the same reasons that caused the BP disaster.

    Something for Neo-Darwinists to consider : Will Neo-Darwinists agree that Neo-Darwinism has been falsified if functions are found for the introns not now known to have functions?

  103. 103

    tribune7

    The Deepwater Horizon disaster wasn’t the fault of BP engineers who issued warnings about the practices in place but with the corporate management and political regulators (yes this means Obama) who made decisions apparently based on hubris and greed.

    So it’s Obama’s fault? What specific decision did Obama make before this event that can be said to have caused it?

    Something for Neo-Darwinists to consider : Will Neo-Darwinists agree that Neo-Darwinism has been falsified if functions are found for the introns not now known to have functions?

    Even if Neo-Darwinism were to be falsified in such a manner how does that support ID? Disproving A does not support B!

    What’s the ID prediction for introns? That they all have function? 50% have function? 1% has function? What? That prediction is not clear to me from reading this entire thread.

  104. BP engineers who issued warnings about the practices in place but with the corporate management and political regulators (yes this means Obama) who made decisions apparently based on hubris and greed. . . .So it’s Obama’s fault?

    What an ironic way of phrasing it :-) Yes, it is partly Obama’s fault

    That does not, btw, exempt the corporate leaders who appeared to have ignored the warnings from their engineers whom my initial post was defending.

    Even if Neo-Darwinism were to be falsified in such a manner how does that support ID?

    If one party predicts a thing will happen — say a function will never be found for a particular intron — and the other party predicts the opposite and it should come to pass, the party making the successful prediction will gain credibility at the expense of the other.

    You are correct, though, in that falsifying Neo-Darwinism does not prove ID.

  105. 105

    tribune7

    If one party predicts a thing will happen — say a function will never be found for a particular intron — and the other party predicts the opposite and it should come to pass, the party making the successful prediction will gain credibility at the expense of the other.

    Can I pin you down on the specifics of that? What’s the (your) ID prediction for introns in general?

    That they all have function? 50% have function? 1% has function?

  106. Can I pin you down on the specifics of that? What’s the (your) ID prediction for introns in general?

    That they all have function? 50% have function? 1% has function?

    That most or 50% plus will be found to have function.

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