Intelligent Design

The Sound of Mendelian Genetics Exploding

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Rogue weeds defy rules of genetics

Explosion
Other biologists are astonished by the findings. “It’s amazing,” says David Baulcombe, an expert on plant RNA at the John Innes Centre in Norwich, UK. “The notion that RNA carries the information almost seems like the only way it could happen.”

Recent experiments cause a central tenet of NDE to miss the prediction again. Genes not found in the parents but found in earlier ancestors are somehow preserved (stored in unexpressed form) and show up again in later generations.

This is a good avenue for positive ID research. Planning for the future with genomic information is a central tenet of the ID front loading hypothesis. Lack of any known means of conserving unexpressed genetic information is the major objection lobbed at the front loading hypothesis. Natural selection is the only mechanism known for preserving genomic information and to do it the information must be “expressed” so that it has some testable survival value for selection to act upon. If it’s not expressed then it is subject to eventual destruction by natural selection’s ever present companion “random mutation”. Evidently there is a means of preserving unexpressed information after all. See also this related blog article I wrote two months ago which is even stronger evidence of a genetic information cold-storage mechanism: The Sound of Circular Reasoning Exploding.

Rogue weeds defy rules of genetics
00:01 23 March 2005
NewScientist.com news service
Andy Coghlan

Mendelian inheritance, the central tenet of genetics, is under attack from a few scrawny weeds that have not read the textbooks. The weeds are somehow inheriting DNA sequences from their grandparents that neither of their parents possessed – which is supposed to be impossible.

The orthodox view is that genes are passed down in the form of DNA, and all organisms have to make do with this parental DNA inheritance, mutations and all. Chemical or structural modifications to DNA can switch off genes, and these changes can pass from generation to generation, a phenomenon called epigenesis. But epigenetic changes do not alter the actual sequence of DNA.

Yet that is what seems to occur in the weedy cress Arabidopsis thaliana, the workhorse of plant biologists. Cress with two mutant copies of one gene seem to be able to correct the DNA they pass on, ensuring that at least a few of their offspring revert to normal. Robert Pruitt, whose team at Purdue University in West Lafayette, Indiana, US, made this extraordinary discovery, thinks that the mutant genes are being repaired using RNA templates inherited from earlier generations.

Other biologists are astonished by the findings. “It’s amazing,” says David Baulcombe, an expert on plant RNA at the John Innes Centre in Norwich, UK. “The notion that RNA carries the information almost seems like the only way it could happen.”

RNA back-ups
It is possible that the phenomenon is limited to this one plant. But in Nature (vol 434, p 505), Pruitt’s team speculates that it might be a more widespread mechanism that allows plants to “experiment” with new mutations while keeping RNA spares as a back-up.

If the mutations prove harmful, some plants in the next generation revert to their grandparents’ DNA sequence with the help of the RNA. “It does make sense,” Pruitt says.

Such a mechanism would be especially useful to plants that self-pollinate and so are not as genetically variable as other plants. But it might happen in all plants and even animals.

Use the link at the top for the full article. HT to GilbertT and Jean Staune for alerting me to this and its connection with ID front loading.

22 Replies to “The Sound of Mendelian Genetics Exploding

  1. 1
    johnnyb says:

    I think the paper they are referring to is here.

  2. 2
    Michaels7 says:

    Hmmm, maybe this is a silly question. But, if it reverts back, 10% that is, then are we essentially looking at a self-correcting mechanism that defies any type of RM&NS mechanisms for macro changes that are not programmed?

    This goes back to Degneration. Mutations are allowed, but degenerate. While mechanisms exist to bring back original code.

    That’s bizarre unless by Design.

    I wonder if light has anything to do with it, fractals. Light to matter, matter to light.

    http://www.physorg.com/news90077438.html
    Physicists unite light and matter.

    Differing spectrums of Light grows life, and mutates life. Can light repair life?

  3. 3
    Jason Rennie says:

    Oh come on Dave don’t be silly. All of this makes perfect sense and is a prediction of the standard darwinian paradigm. How could you be so foolish as to think otherwise ?

    Clearly the mechanism at work is magic. It is as simple as that. You can be so dense at times Dave

    😛

  4. 4
    Joseph says:

    More layers of information.

    Yup blind and purposeless watchmakers do that sort of thing daily. Jason is right (LoL!)

  5. 5
    Art2 says:

    There’s more (and less) to the story:

    One alternative hypothesis.

    And some follow-up studies.

    I know we’re all for the RNA World (and the RNA Underworld) here, but Lolle et al. may be a bit premature.

  6. 6
    shaner74 says:

    “Clearly the mechanism at work is magic. It is as simple as that. You can be so dense at times Dave”

    hehe, yeah, everyone on UD is “dense” At least, that seems to be the consensus among the “science” (laughs) blogs. This is incredible though; plants may have the ability to “experiment” with new designs, while keeping a backup just in case?? Wow! This article here speaks of RNA transferring heritable traits in mice:

    http://www.the-scientist.com/news/display/23494/

  7. 7
    JGuy says:

    What would Theodosius Dobzhansky say? 😛

  8. 8
    Joseph says:

    And just to stick up for Mendel-

    He never did deny such a thing. He was aware that some trait(s) can skip generations. Obviously he didn’t know the detail because the technology didn’t exist to observe it.

    And just because until now we thought we knew the “only” mecahnism responsible, that may be a reflection on us (humans) and our research methodology, as opposed to anything Mendel provided us as a platform from which to proceed.

    IOW great article but just a little easier on Mendel (just a thought). 😉

  9. 9
    jerry says:

    I do not think Mendel is under attack as the article says. Like everything else in science, we see there are multiple layers of explanation and here is an additional mechanism for transmitting genetic data. It appears to saying that these new findings supplement Mendelian genetics not replaces it.

    Newtonian physics is still alive and well in today’s world even though it doesn’t explain everything.

  10. 10
    Atom says:

    You guys are missing the obvious explanation:

    A plant randomly mutates to make back-up copies of it’s DNA on RNA strands. This mechanism can come about in one swoop, or gradually, though it doesn’t have a selection value. How does it do it? Science™ is working on it, and your incredulity is no argument against it.

    Ok, so now we have these useless RNA strands, they become fixed in the population…by drift. Then another random mutation happens that allows the RNA strands to repair DNA strands. This obviously has a selection value (since we all have a well-defined model of the fitness landscape, we can say this with assurance.) Thus, it quickly becomes fixed in the population.

    Bingo!

    Ok, sure I hand-waved by assuming the mutations were beneficial or could become fixed in the population in the time alloted, and were within the range of random combinatorics to reach. Those are just details. The narrative is what Science™ is all about. Now I can publish my story in Nature. (Or at least on PT) : )

  11. 11
    Jehu says:

    How does it do it? Scienceâ„¢ is working on it, and your incredulity is no argument against it.

    LOL! maybe you should copryight that argument.

    I can’t help noticing tat this whole thing is an evolution stopper. But not to worry, they offer the secret handshake

    Pruitt’s team speculates that it might be a more widespread mechanism that allows plants to “experiment” with new mutations while keeping RNA spares as a back-up.

    If the mutations prove harmful, some plants in the next generation revert to their grandparents’ DNA sequence with the help of the RNA. “It does make sense,” Pruitt says.

    How would the plant “know” that the mutation is “harmful” or “successful”? Do the plants take a population census to determine the fixation rate of the new mutation?

  12. 12
    Atom says:

    Do the plants take a population census to determine the fixation rate of the new mutation?

    LMAO! Good point. It checks gene frequencies. 😉

  13. 13
    PaV says:

    In response to post #2, the first reference is from Reed Cartwright of PT fame–not exactly neutral in all this. And here’s Lolle’s reply to the Peng article:

    http://www-plb.ucdavis.edu/Lab.....06Peng.pdf (scroll down to view the reply)

    Here’s part of their reply that takes the air out of Cartwright’s approach, and that points to super-Mendelian mechanism at work:

    We have also examined more extensive
    patterns of inheritance of single-nucleotide
    polymorphisms in F2 populations, similar
    to those we originally described2. These patterns
    of inheritance are also inconsistent with
    an outcrossing explanation because there was
    no single male parent present that could have
    provided the combination of non-parental
    alleles observed in the ‘restored’ progeny.
    Furthermore, the results indicate that genetic
    restoration of ancestral alleles can take
    place in HTH/hth heterozygotes; these plants
    have a floral morphology identical to wild
    type and therefore would not be expected to
    show increased outcrossing (J.M.Y., R.E.P.
    and S.J.L., unpublished results).

  14. 14
    Art2 says:

    PaV, Lolle et al.’s letter doesn’t address Comai and Cartwright. (And it is patently absurd to suggest that Comai and Cartwright’s letter was published because The Plant Cell is biased aginst Lolle et al., or that Cartwright was an author.)

    Here’s the closing paragraph from Lolle et al.’s reply – as we see, outcrossing is not ruled out as an explanation of the hothead phenomenon. Moreover, Lolle et al. really do not rule out the alternative explanation, as they cannot at all explain Peng et al. The latter authors, OTOH, come closer to explaining the observations.

    In summary, the outcrossing explanation
    proposed by Peng et al.1 is a reasonable hypothesis
    to explain some of the data associated
    with hothead genetics, and indeed is one of the
    first that we considered. Ultimately, we discarded
    this explanation because it was inconsistent
    with many of our experimental results.
    However, the results of Peng et al. show that,
    at least under some growth conditions, outcrossing
    in hth/hth plants remains an issue that
    needs to be taken into account.

  15. 15
    PaV says:

    Art2: “PaV, Lolle et al.’s letter doesn’t address Comai and Cartwright.”

    Are you trying to say that they don’t mention Comai and Cartwright by name? Is that your point?

    “(And it is patently absurd to suggest that Comai and Cartwright’s letter was published because The Plant Cell is biased aginst Lolle et al., or that Cartwright was an author.)”

    This comment of yours seems patently absurd. OTOH, it is not, in the least, absurd to question someone like Cartwright’s motives. I’ve posted on PT. I know the kind of attitude they have, the religious fervor that drives them. So, frankly, I’m not too interested in his opinion. Their putative hypothesis does not correlate well with some of the results that Lolle, et. al. report, despite their protestations otherwise. The paper has the tone of someone who is desperately trying to save genetics: “Our mutator hypothesis may appear complicated, but it comports with the data.” Ever hear of Occham’s Razor?

    “Moreover, Lolle et al. really do not rule out the alternative explanation, as they cannot at all explain Peng et al.”

    You don’t seem to understand the implications of the very paragraph you’re quoting. What is it about “ultimately, we discarded this explanation because it was inconsistent with many of our experimental results” that’s so difficult to understand?

  16. 16
    Art2 says:

    PaV, I understand quite well the two papers I have cited and read. Just what is it about the statement “However, the results of Peng et al. show that,
at least under some growth conditions, outcrossing
in hth/hth plants remains an issue that
needs to be taken into account” that you don’t get.

    Let’s review for readers who haven’t the time or resources to dig up the papers. Lolle et al. observed a curious elevated frequency of reversion of a particular Arabidopsis mutation, at the Hothead locus. They also found that the reversion was not due to elevated point mutation at the locus (or globally, I presume), but rather due to exact and frequent re-introduction of large swaths of the wild-type genome. They were studying homozygous mutants that would not seem to have a “reservoir” of wild-type chromosomes to call upon. Hence the suggestion of some other mechanism, perhaps a hidden collection of RNA that together represents entire genomes. Somehow, these authors hypothesized, this RNA reservoir gets recruited to facilitate replacement with the wild-type genes, in plants that have no corresponding chromosomal DNA content.

    Peng et al. set out to repeat the experiment. Not, mind you, because they are part of the evolutionist cabal and had to defend the faith. But rather because they wanted to be on in the lead wave of studying yet another RNA (under)world-related phenomenon. (After all, RNA is the path to glory and prize in molecular biology, and if you have a chance to get in on the ground floor, you take it.) Unfortunately, Peng et al. could not repeat Lolle et al.’s study. What Peng et al. apparently did differently was to perform studies with hth homozygous plants in complete isolation from all other plant lines. Under these conditions, they saw no elevated reversion rate. This suggested outcrossing as a possible explanation of Lolle et al. Peng et al. tested this, by putting hth mutants in places along with other lines, ones tagged with one or more markers they could follow (they had more than one possible pollen donor in this study). Lo and behold, they saw elevated reversion, but all the revertants also had the marker genes (genes that have never, ever been in the lineages leading to the hth mutants). In other words, reversion was due to outcrosssing.

    Arabidopsis is normally a self-crosser; outcrossing is rare with normal plants. Given the genetic and molecular analyses of Lolle et al., outcrossing didn’t seem very likely. But Peng et al. shows otherwise. Comai and Cartwright, while they did not explicitly mention outcrossing, actually provide one theme (if not exact mechanism) for the elevated contributions of outcrossing to the behavior of this mutant. Readers should read their letter and think about it. (It hasn’t anything to due with the possible mutageneic effects of the hth mutation, as Comai and Cartwright propose, but rather with the metabolic consequences that Comai and Cartwrigt mention, and resulting effects on reproductive fitness.)

    Where we stand at the moment – Peng et al. call into serious question the study, and more importantly the conclusions and hypothesis, that Baulcombe mentions in DaveScot’s blog entry. As Lolle et al. state in the response to Peng et al., there are still some curious genetic contradictions in their plants. But, given Peng et al., it seems most likely that even these occurrences will be due to pretty standard Mendelian mechanisms. In a nutshell, if the hth mutant only reverts when grown in the same locale as other wild-type plants, then outcrossing (a pretty standard Mendelian genetic mechanism) is most probably involved in the “reversion”.

  17. 17
    jerry says:

    Art2,

    Is this an accurate assessment: the plants in question did not exhibit a reversion to a previous allele/gene that had been lost when these plants were grown in isolation but when they were grown in some proximity with plants having the lost allele they then re-acquired it. The obvious assumption is that they somehow got it from the nearby plants.

    If this is true, then isn’t this really sloppy experimentation?

  18. 18
    Art2 says:

    Hi jerry,

    You have the basic gist of things. I wouldn’t call this a case of sloppiness, though. Many people over the years have done genetics experiments in conditions similar to those described by Lolle et al. without seeing untoward apparent reversion frequencies. That’s what made this one set of results stand out. This controversy has nothing to do with sloppiness, and everything to do with the effects of the hth mutation.

    IMO, hth is telling us some new and interesting things about plant reproductive biology. But, as Lolle et al. are saying, it’s not all one neat package yet. Stay tuned.

  19. 19
    PaV says:

    Art2:
    PaV, I understand quite well the two papers I have cited and read. Just what is it about the statement “However, the results of Peng et al. show that,
at least under some growth conditions, outcrossing
in hth/hth plants remains an issue that
needs to be taken into account” that you don’t get.

    That Lolle, et. al. say that “at least under some growth conditions, outcrossing in hth/hth plants remains an issue that needs to be taken into account”, shouldn’t be taken as a concession.

    In your post, you present a very good overview; however, you’re apparently not interested in Lolle, et. al.’s response:

    Here’s part of what they say:

    Outcrossing was a possibility
    that we thoroughly explored early on in our investigation, but we discounted it as an explanation because it was inconsistent with
    many of our experimental results.

    We described two experiments that were inconsistent with outcrossing: one in which there was transmission of a wild-type HTH allele from a homozygous mutant (hth/hth)
    male parent, and another in which there was
    recovery of homozygous wild-type (HTH/HTH) embryos dissected from homozygous mutant(hth/hth)parents. In further experiments that were similar, but not identical, to those described by Peng et al.1, we did see reversion in hth/hth homozygotes grown in isolation (results not shown).
    (N.B. This directly contradicts Peng, et. al.)

    Peng, et. al.’s results seem to be no more than a caveat in the discussion of Lolle, et. al.’s results. With that caveat aside, Lolle, et. al.’s results still stand.

  20. 20
    PaV says:

    In the last post, I underlined several sections in the quote, but somehow it disappeared when I posted it. Note, especially, the word “inconsistent” and what follows.

  21. 21

    Put this in the wrong thread.

    “If the mutations prove harmful, some plants in the next generation revert to their grandparents’ DNA sequence with the help of the RNA. “It does make sense,” Pruitt says.

    Such a mechanism would be especially useful to plants that self-pollinate and so are not as genetically variable as other plants. But it might happen in all plants and even animals.”

    This is a big problem, in my thinking, for Darwinism. The overall Darwinian process creates advantages through mutational errors. That system, hypothetically, creates an error-control mechanism which runs counter to the overall mechanism.

  22. 22
    TomT says:

    http://www.fieldmuseum.org/exh.....pexhib.htm

    The new Mendel exibit at the field museum shows this discovery. I was just there a month a go. It didn’t go into detail on this finding, but it did have an article on display about it.

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