Biology Genomics Intelligent Design Irreducible Complexity Origin Of Life

DNA Preservation discovery wins Nobel prize

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Were one to design the encoded DNA “blueprint” of life, would not one incorporate ways to preserve that “blueprint”? The Nobel prize in medicine has just been awarded for discovery of features that look amazingly like design to preserve chromosomes. See:

3 Americans win medicine Nobel for chromosome research

Three U.S. researchers were awarded the 2009 Nobel Prize in Physiology or Medicine for their work on how chromosomes are protected against degradation, the Nobel Foundation reported Monday.
The Nobel Assembly announces the winners of the prize in medicine Monday in Stockholm, Sweden.

The Nobel Assembly announces the winners of the prize in medicine Monday in Stockholm, Sweden.

Elizabeth H. Blackburn, Carol W. Greider and Jack W. Szostak will share the $1.4 million prize for research on structures at the end of chromosomes called telomeres and on an enzyme that forms them, called telomerase.

The long, thread-like DNA molecules that carry genes are packed into chromosomes. Telomeres are the caps on the ends of chromosomes. Blackburn and Szostak discovered that a unique DNA sequence in the telomeres protects the chromosomes from degradation, the Nobel announcement said. Greider and Blackburn identified telomerase, the enzyme that makes telomere DNA. These discoveries explained how the ends of the chromosomes are protected by the telomeres and that they are built by telomerase.

If the telomeres are shortened, cells age. Conversely, high telomerase activity leads to telomere length being maintained and the delay of cellular degradation. That is the case with cancer cells, which do not degrade easily. Certain inherited diseases, in contrast, are characterized by a defective telomerase, which results in damaged cells.. . .

See interviews with the Nobel Committee announcement

These telomeres can probably be shown to be essential to survival, and are likely to be irreducibly complex. If so, how can macro evolution explain the origin of this marvelous preservation feature that appears to be an Intelligent Design?

31 Replies to “DNA Preservation discovery wins Nobel prize

  1. 1
    ellazimm says:

    Too bad no one from the ID camp predicted this discovery.

    Perhaps someone will weigh in on whether or not it IS irreducibly complex.

  2. 2
    Borne says:

    ellazimm:

    Too bad no one from the ID camp predicted this discovery.

    Perhaps.

    Did anyone from the Darwin camp? I doubt it.

    Yet this is exactly the kind of thing ID would predict – stability and protection mechanisms.

    Darwinian theory could not predict this since it implies an underlying knowledge of genetic thermodynamics or genetic entropy as well as teleology.

    No underlying teleology, no predictions of protection or correction mechanisms.

    Also, no theory can predict everything (although Darwinists will certainly try to ‘post hoc’ this one as usual with some twisted logic as usual).

  3. 3
    tragic mishap says:

    If you wanna do your jumping jacks and wave your pom-poms around, that’s fine. Stay off the field.

  4. 4
    Arthur Hunt says:

    Thank you, RNA World.

  5. 5
    Borne says:

    tragic mishap: who are you talking to and what exactly do you mean please?

  6. 6
    hdx says:

    “Telomerase is an independent mechanism. It adds DNA to the ends of chromosomes to take care of this sad glitch. It saves the chromosomes bacon. Its not elegant or clever. In fact, its kind of clumsy. But it works and has done so for billion of years for every creature, apart from bacteria. They have circular DNA.”

    Elizabeth Blackburn went further into the biology of telomerase. “It’s RNA plus protein which together become a crude little copying machine,” she says. “It’s thought to be one of lifes ancient relics which got fossilised into our cells. Had it been useless, it would have been selected out.”

    Blackburn doesn’t think the system was intelligently designed.

    http://grants.innovation.gov.a.....ckburn.htm

  7. 7
    DNA_Jock says:

    Yes, Borne, the Darwin camp predicted telomeres: when they elucidated the mechanism of DNA replication, they said “There’s a problem with the ends of linear chromosomes, they should get shorter and shorter, there must be some mechanism that protects the ends…” So they went and looked at the end of linear chromosomes, and found telomeres. And they built artificial chromosomes from scratch, and did all sorts of experiments and found telomerase and new targets for cancer therapies etc, etc.
    And, DLH, anyone who knows anything about biology knows that telomeres are not “essential to survival”: bacteria don’t have them.

  8. 8
    Borne says:

    DNA_Jock:

    Yes, Borne, the Darwin camp predicted telomeres

    I’m afraid you missed the point entirely.

    We’re not talking about the prediction or discovery of telemerees at all but as per the article

    Blackburn and Szostak discovered that a unique DNA sequence in the telomeres protects the chromosomes from degradation

    Also, Darwinian theory itself played absolutely no role in the discovery of telemeres in the first place.
    I hope you can see the difference between a prediction based on Darwinian theory and one based entirely upon logic in view of observations.

  9. 9
    tragic mishap says:

    Talking to ellazimm, Borne. Half his posts take the following form,

    “Rah, rah, siscoombah!
    ID sucks and Darwin rocks!”

  10. 10
    Borne says:

    hdx :

    Blackburn doesn’t think the system was intelligently designed.

    So what? Dawkins doesn’t believe in God and I don’t believe in neo Darwinism or pink and yellow Plutonian horses.

    What anyone believes changes nothing of facts.

    They’re merely towing the party line with the traditional hat tip to Darwin and nose up to ID.

    As for their ‘not clever’, ‘kind of clumsy’…

    How much you to bet that they swallow those words when they start digging deeper?

    Darwinists, since day one, have always claimed things were simple – they’ve ALWAYS been wrong.

  11. 11
    Borne says:

    tragic mishap: Just half?! 😉

  12. 12
    computerist says:

    I’m not sure of any explicit predictions made by the ID community regarding this, but John A. Davison’s published papers (PEH and SMH) are fairly inline with these findings. John A. Davison argues that chromosomes are conserved and chromosome positions effects are determined as well as responsible for most of evolutionary change rather than NS & RM.

  13. 13
    hdx says:

    @1

    Did anyone from the Darwin camp? I doubt it.

    Yes James Watson was the first to predict that there would be some mechanism to restore ends.

  14. 14
    DNA_Jock says:

    Borne, in your response to ellazimm’s comment that “no one from the ID camp predicted this” you claimed that “this discovery” was “exactly the the kind of thing ID would predict”, and asked “Did anyone from the Darwin camp? I doubt it. ”

    In my reply, I note that people in the “Darwin camp” went looking for telomeres. What, exactly, is the point that I am missing? What, precisely, is the prediction that ID would have made [Always with the subjective…] but evolutionary theory did not? And you need to be very specific here – “genetic thermodynamics” is gobbledegook.

    I also enjoyed your wisecrack “How much you to bet that they swallow those words [about the system being clumsy] when they start digging deeper?”
    You do know that telomeres were characterized over 25 years ago, and research on them has never stopped? How deep would you like them to dig?

  15. 15
    hdx says:

    @2

    Yet this is exactly the kind of thing ID would predict – stability and protection mechanisms.

    And why wouldn’t Darwinian evolution have these these things?

    My question is why would an intelligent designer not design a polymerase that could replicate to the ends of DNA strands instead of creating some whole new mechanism because the DNA replication machinery is flawed?

    @9

    Darwinists, since day one, have always claimed things were simple – they’ve ALWAYS been wrong.

    Um no and no. The very fact that you need the telomeres makes things more complicated than they need to be. Lots of biology is a mess and not simple.

    What anyone believes changes nothing of facts.

    Blackburn has been performing scientific experiment in this are for around 30 years, this is very different than someones belief in God. You talk about facts, yet but there are no facts here to support telomeres/telomerases are a product of intelligent design. Read some of her articles and reviews and you can see the facts she relies on.

    Here is an additional review
    http://www.springerlink.com/co.....lltext.pdf

    One other question to ask, why would an intelligent designer place telomeres within the middle of a chromosome?

  16. 16
    ellazimm says:

    Tragic Mishap: I’m sorry you see it that way. I will try harder to be more respectful.

    I do think ID needs to put itself out more regarding research, publication and predictions. I’d like to see it spend more time and energy on research. If 60% of the American public question evolution as a viable explanation for the diversity of life on Earth then surely it would be possible to fund a lot of research outside of regular academic circles. I am encouraging all ID proponents to push for that to happen.

  17. 17
    DLH says:

    DNA_Jock at 7
    Regarding bacteria, to be more precise – most eukaryotic organisms, a few procaryotes and a few bacteria have telomeres.

    Cancer and aging: The importance of telomeres in genome maintenance Francis Rodier et al. 2004 LBL Paper LBNL-56548

    Functional telomeres are essential for maintaining the integrity and stability of genomes. When combined with loss of cell cycle checkpoint controls, telomere dysfunction can lead to genomic instability, a common cause and hallmark of cancer. Consequently, normal mammalian cells respond to dysfunctional telomeres by undergoing apoptosis (programmed cell death) or cellular senescence (permanent cell cycle arrest), two cellular tumor suppressor mechanisms.

    Preventing cancer appears to be rather useful!

    With a quick search you will likely find more research detailing telomeres as “essential”.

    Google Scholar lists some 17,500 hits for “telomere essential”.

    e.g. see: Telomerase is Essential to Alleviate Pif1-induced Replication Stress at Telomeres etc.
    Michael Chang et al.

    ABSTRACT
    Pif1, an evolutionarily conserved helicase, negatively regulates telomere length by removing telomerase from chromosome ends. Pif1 has also been implicated in DNA replication processes such as Okazaki fragment maturation and replication fork pausing. We find that overexpression of PIF1 results in dose-dependent growth inhibition. Strong overexpression causes re-localization of the DNA damage response factors Rfa1 and Mre11 into nuclear foci and activation of the Rad53 DNA damage checkpoint kinase, indicating that the toxicity is caused by accumulation of DNA damage. We screened the complete set of ~4800 haploid gene deletion mutants and found that moderate overexpression of PIF1, which is only mildly toxic on its own, causes growth defects in strains with mutations in genes involved in DNA replication and the DNA damage response. Interestingly, we find that telomerase-deficient strains are also sensitive to PIF1 overexpression. Our data are consistent with a model whereby increased levels of Pif1 interfere with DNA replication, causing collapsed replication forks. At chromosome ends, collapsed forks result in truncated telomeres that must be rapidly elongated by telomerase to maintain viability.

    This shows that it is not just the presence/absence of gene expression that is critically important, but also the degree of gene expression. How do you propose a quantitative gene expression level by random mutation, when all such mutations from the “design” value fail to maintain “viability”?

  18. 18
    tragic mishap says:

    I’m glad you feel that way ellazimm. Here’s a link so you can help:

    http://www.discovery.org/csc/donate.php

  19. 19
    DNA_Jock says:

    I apologize, DLH, for my simplification. When I said

    And, DLH, anyone who knows anything about biology knows that telomeres are not “essential to survival”: bacteria don’t have them.

    I thought you would understand from the context that the existence of one viable species without telomeres is sufficient to refute your claim that they are “essential to survival”.
    The existence of bacteria with and without telomeres does raise an interesting point though – how did life transition from the telomere-free life of 99% of bacteria (and archaea) to the telomere-dependent life of streptomyces, fungi, plants and animals. Tough for Darwinists to explain, unless bacteria had non-essential extra-chromosomal DNA, which could exist in circular form or linear form. Oh well.
    Thank you for the link to Rodney Rothstein’s latest work (btw he and Jack S came up with the DSBR model of recombination), but the idea that telomeres have subsequently become important, even essential, in eukaryotes is hardly relevant to whether they could have arisen via evolution.
    Also, you may not have noticed,

    Preventing cancer appears to be rather useful!

    but there is little evolutionary selection against late-in-life cancer. Hence all the research…

  20. 20
    TelomereGirl says:

    I’m sorry, but as a telomere researcher I feel a need to step in here. DLH COMPLETELY mis-represents the Chang et al paper he posted above-

    This shows that it is not just the presence/absence of gene expression that is critically important, but also the degree of gene expression. How do you propose a quantitative gene expression level by random mutation, when all such mutations from the “design” value fail to maintain “viability”?

    No biologist would argue with the statement that levels of gene expression are important. Even if it were true that “all the designed mutations fail to maintain viability” (which even just from reading the abstract is patently untrue- lying doesn’t help your cause DLH), this presents no trouble for natural selection.

    If a protein picks up a new function, it may help its descendants and they grow faster/reproduce more. If expression levels increase to the point that they’re harmful (as can apparently happen in Pif), fitness goes back down and there are fewer or no descendents. If the ones with a moderate level of this new gene reproduce a lot and the ones with too much or too little reproduce less- voila! The appearance of tuning and design, all from natural selection.

  21. 21
    DLH says:

    DNA_Jock at 19
    “there is little evolutionary selection against late-in-life cancer.”
    All the greater reason to see this as ID as Darwinism has no explanation for systems with such obvious lack of “evolutionary selection”.

    “the existence of one viable species without telomeres is sufficient to refute your claim that they are “essential to survival”.”

    Conversely, the greater the complexity of the organism, the greater need to preserve the design/DNA for which Darwinism has no explanation.

    See Genetic Entropy and the Mystery of the Universe, John C. Sanford 2005 ISBN-13: 978-1599190020.

    Recommend you try your hand at Mendel’s Accountant
    Explore for yourself the accumulation of mutations under all realistic parameters.

  22. 22
    TempHut says:

    DNA_Jock at 19
    “there is little evolutionary selection against late-in-life cancer.”

    DLH at 21
    “All the greater reason to see this as ID as Darwinism has no explanation for systems with such obvious lack of “evolutionary selection”.

    Huh? Late in life cancer is pretty common (much more so than in child bearing years and earlier) and not something that we can expect evolution to solve since it happens after a person has offspring. ID is left with the difficult question of why the designer did so much more to prevent early in life cancer than late in life cancer.

  23. 23
    DLH says:

    TelomereGirl at 20
    Good to have an expert weigh in on issues. Apologies for misunderstanding an overstating: “all” rather than “some mutations fail to maintain viability” on rapidly reading the abstract.

    On further reading, Cheng stated: “. . moderate over expression of PIF1, which is only mildly toxic on its own, causes growth defects in strains with mutations in genes involved in DNA replication and the DNA damage response.”

    i.e., Overexpression of PIF1 compounds other mutations.

    Further Cheng et al.

    “DNA damage caused by high levels of Pif2 induce the accumulation of ssDNA. . . the damage is not specifically localized to telomeres. . .

    . . .Pif1 removes telomerase from telomeres and DNA DSBs . . . overexpression of PIF1 inhibits cell growth in a dose dependent manner. . . .
    Elevated levels of Pif2 interfere with DNA replication: . . . overexpression of PIF1 is toxic to . . . mutants with defects in lagging strand synthesis. . .
    . . .our studies strongly suggest that elevated levels of Pif1 disrupt lagging strand DNA synthesis . . .
    . . .deletion of several kinetochore genes renders cells sensitive to PIF1 overexpression (Table 2). . .”

    “…our work shows the importance of carefully regulating the protein levels of Pif1 in the cell. We propose that overexpression of PIF1 impairs lagging strand synthesis resulting in DNA damage. At telomeres, telomerase activity is needed to repair this damage.”

    —————

    You claimed: “If a protein picks up a new function, it may help its descendants and they grow faster/reproduce more.”
    That is an astronomically big “IF”.

    Neo-Darwinian evolution has to demonstrate how complex systems come to be formed by random mutations when there are such harmful effects until the those complex systems are in place.

    Degradations by mutations from normal base operation would be expected from ID.

    Please review the population models reviewed in Genetic Entropy and the Mystery of the Universe.
    Please try your hand at Mendel’s Accountant.
    See if you can find any way under realistic parameters how the numerous mutations needed to create PIF1 and telomerase, compared to dominance of accumulated “neutral” and harmful mutations.

    PS My misunderstanding that all mutations were not viable does not constitute “lying”. Please refrain from accusations of moral perversity when you have no clear evidence.

  24. 24
    DLH says:

    DNA_Jock

    ID is left with the difficult question of why the designer did so much more to prevent early in life cancer than late in life cancer.

    Would it not make sense that design provides greater effort to preserve the design on to the next generation?
    There are also extensive systems to repair DNA damage that fit in with the ID perspective. NeoDarwinism has the severe challenge of explaining how any of those complex systems came into being with random mutations and “selection”, on top of its huge presupposition of the incredible complexity of self reproducing cells. It has

    Distinguish between the problem of suffering versus that of preserving the species.

  25. 25
    Winston Macchi says:

    So when a Darwinist looks at something and decides that it would be “bad design” and then uses that as an argument against ID you (I would say rightly) tell them that argument is flawed.

    When an IDist looks at something and considers it as “good design”, that is now a nice little pro-ID argument? Consider me confused.

  26. 26
    DNA_Jock says:

    DLH,
    Before I pony up any of my cash for the book that you keep touting here, perhaps you could answer a couple of questions for me.

    Previous UD posts indicate that Behe, Dembski and Johnson have all endorsed this book. Is this true?

    One of the glowing Amazon reviews states:

    Sanford concludes that the degeneration of the genome is unstoppable and Darwinism could never have gotten off the ground. Contrary to one reviewer’s beliefs about this book, Sanford only spends a few paragraphs on the declining life-spans of the generations of men after Noah. He shows that the life-spans of post-flood man, as recorded in the Bible, follow a curve that is eerily similar to a declining fitness curve found in earlier chapters of this book.

    Is this statement accurate?

    Thanks

  27. 27
    osteonectin says:

    Do telomere sequences contain CSI/FSCI? And where does it come from provided that a single telomere repeat (TTAGGG) is quite short.

  28. 28
    DLH says:

    DNA_Jock
    That paragraph appears reasonable.

    Sanford spends most of the book systematically going through the consequences of known genetic processes and the major population models.
    1) The genome is the book of life. Where did it come from?
    2) Are mutations good?
    3) How much mutation is too much?
    4) All-powerful Selection to the rescue?
    5) Can Genomic Selection problems be solved?
    6) A closer look at noise.
    7) Crow to the rescue?
    8) Man to the rescue?
    9) Can natural selection create?
    10) Is the downward curve real?
    Personal Postlude What Hope?
    Appendix 1 What other scientists say
    Appendix 2 How many mutations can be selected against simultaneously?
    Appendix 3 The phenomenon of Unity, and the concept of Integrated Complexity.
    Appendix 4 Three Possible Objections
    References

    In Appendix 1 Sanford reviews the major population models and their consequences.

    Sanford has one figure “Declining Lifespan – Noah’s descendants” with a paragraph including:
    “we see a dramatic decline in life expectancy, which has the strong appearance of a biological decay curve. Fitting the data to the “line of best fit” reveals an exponential curve following the formula: y=5029.2*x^-1.43. The curve fits the data very well – having a correlation coefficient of 0.90.”
    —————-
    See Scordova’s review on endorsements:
    On the Snaford’s back cover:

    In the Mystery of the Genome Cornell University researcher John Sanford lifts the rug to see what evolutionary theory has swept under it. He shows that, not only does Darwinism not have answers for how information got into the genome, it doesn’t even have answers for how it could remain there.

    Michael Behe

    Other back cover endorsements are from John Baumgardner, Henry Morris, and Phillip Johnson.
    ————-
    You can download Mendel’s Accountant for free along with the associated articles.

  29. 29
    DLH says:

    Winston Macchi at 9
    Good question on “bad” vs “good” design.

    The Darwinist’s very accusation of “bad design” implies a recognition that “design” exists – for which the Darwinist has no explanation.

    As an engineer, I usually find the argument of “bad design” comes from a woeful misunderstanding of the design process and a very limited understanding of the science or evidence involved.

    I know of features like the eye that Darwinist’s claim are “bad design” when more detailed understanding of the design requirements, like response speed, provide the design parameters that result in the feature actually being an excellent design.

    “When an IDist looks at something and considers it as “good design”, that is now a nice little pro-ID argument?”

    See “Blink” by Malcolm Gladwell

    Those skilled in design can often quickly recognize a good design but it would take a while to explain.

    The reasons for it being a “good design” would need to be explored in depth to provide the quantitative objective basis for that argument.

  30. 30
    ericB says:

    To TelomereGirl at 20,

    First, thanks for jumping in with some clarification. I hope you continue to participate at UD.

    That said, I would like to comment on your statement:

    “If expression levels increase to the point that they’re harmful (as can apparently happen in Pif), fitness goes back down and there are fewer or no descendents. If the ones with a moderate level of this new gene reproduce a lot and the ones with too much or too little reproduce less- voila! The appearance of tuning and design, all from natural selection.”

    It is clear enough that natural selection can weed out cases where excessive expression has become harmful to reproduction. But the natural selection itself never, ever produces anything at all. It merely filters, weeding out the relative losers. It explains survival, not arrival of new beneficial features.

    To explain the design of any regulatory mechanism within a realistic time and number of generations, it is necessary to account for its appearance. Before it can be preferred by natural selection, it must first appear.

    The question begging assumption is that undirected variations are able to produce any mechanism (regulatory or otherwise) that might be needed or helpful. If this can be done in sufficiently small, incremental and preservable beneficial steps, this is feasible and realistic.

    However to approach it scientifically, it is not enough to merely assume that this small, stepwise, unbroken staircase always exists.

    Have you read Michael Behe’s The Edge of Evolution?

    It turns out that even Richard Dawkins has now (indirectly) acknowledged Behe’s point about how certain kinds of changes can be very difficult to come by.

    Other research has supported Behe’s observations that this process can be actually quite limited, e.g. see the first and second posts in a series.

  31. 31
    ericB says:

    TelomereGirl and others,

    Behe has posted the third and final installment in his series of posts about recent research results supporting his Edge of Evolution position.

    Undirected evolution may not be able to easily to move from one structure even to a related structures.

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