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Biotech Science

Plants May Be Able To Correct Mutated Genes 363

ddutt writes "NY Times is running a story that talks of an exciting new discovery, which, if confirmed, could represent an unprecedented exception to Mendel's laws of inheritance. The discovery involves.. 'plants that possess a corrected version of a defective gene inherited from both their parents, as if some handy backup copy with the right version had been made in the grandparents' generation or earlier.'"
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Plants May Be Able To Correct Mutated Genes

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  • by jwgoerlich ( 661687 ) on Wednesday March 23, 2005 @06:08PM (#12029080) Homepage Journal

    New Scientist has coverage. No registration required.

    http://www.newscientist.com/article.ns?id=dn7185 [newscientist.com]

    J. Wolfgang Goerlich

  • No, not really (Score:5, Informative)

    by Anonymous Coward on Wednesday March 23, 2005 @06:13PM (#12029167)
    For the people who, ah, read the paper, if this particular gene (HTH) is mutated, then a whopping 5% of the second-generation genes manage to revert to the wild type. The other 95% are still mutant. So this mechanism (which is normally masked by the presence of a normal HTH gene) provides for a small number of mutant offspring to revert to wild type, so that a deleterious mutation won't completely destroy the population it occurs in. To disprove "micro-evolution", you'd have to show that this mechanism used to be turned on in every organism and operated at ~100% efficiency rather than 5%. Don't bet on it.

    Now, this is definitely a pretty cool discovery, and there's going to be a stampede of people hunting around looking for some sort of, say, RNA copy of the genome hiding somewhere in Arabidopsis, and there will be a lot of fun in epigenetics. But it isn't going to destroy evolutionary theory, although I expect creationists (excuse me, "intelligent design theorists") will be running around for decades insisting that because this phenomenon exists, it's impossible for mutations to happen.
  • Read the Proper FA (Score:2, Informative)

    by whitehatlurker ( 867714 ) on Wednesday March 23, 2005 @06:15PM (#12029187) Journal
    The original press release [purdue.edu] is at least visible without a subscription. It also has contact information for the author, Robert Pruitt, for those who have inquisitive natures.

    Beware, there are pictures of MUTANT plants here. Watch out for the triffids.

  • by xlurker ( 253257 ) on Wednesday March 23, 2005 @06:17PM (#12029212) Homepage
    just heard this report on NPR.

    What was reported is that although there were mutations in the DNA of the plant, its siblings didn't have them anymore. The researcher said that the best theory at the moment is that the non-mutated DNA was coming from the RNA of the plant. IANAB, but I think RNA usually is though to serve only a functional "middle man" role betweeen the genetic code and the cell machinery, and not actively involved in reproduction...

    He did not say that the plant was actively fixing its DNA for its offspring.

    The non-mutated RNA was itself directly inherted from the parents. In a way the RNA has become a bad backup copy of the DNA. That's the present theory... I guess this is what they'll start looking for... "Bad backup copy" since still 90% of the offspring of the plant still contained the mutated DNA.

  • by Anonymous Coward on Wednesday March 23, 2005 @06:21PM (#12029266)
    Um, I'm sitting here with a copy of the paper in my hand, and Lolle and Pruitt are explicitly marked as having "contributed equally to this work". Furthermore, looking at the departmental web page, Pruitt appears to be the most senior author: he's an associate professor (faculty), whereas Lolle is a research associate (staff). I don't think it's unnatural that they're interviewing the most senior person.
  • by shawb ( 16347 ) on Wednesday March 23, 2005 @06:23PM (#12029293)
    Think of it this way: this ability stems from a mutation in and of itself. All that it does is checks for a flaw in a certain sequence and fixes it. Probably this particular sequence has a high probability of being detrimentally mutated, and so having the repair mechanism makes it more likely that when the mutation happens, it won't kill the whole organism.

    An organism repairing it's own DNA is not unheard of. There are certain somatic (IE: not passed down from generation to generation) mutations and other varieties of DNA damage that lead to cancer. There is a mechanism in place to replace these mutations with another copy. The body also has a way of detecting and removing some viruses and retroviruses that have embedded themselves in the DNA of the host organism, to a limited extent.
  • Same story, no reg (Score:2, Informative)

    by statemachine ( 840641 ) on Wednesday March 23, 2005 @06:38PM (#12029471)
    AP wire story via Yahoo. No registration required.

    Plants Challenge Genetic Inheritance Laws [yahoo.com]
  • by evought ( 709897 ) <evought.pobox@com> on Wednesday March 23, 2005 @06:38PM (#12029473) Homepage Journal
    It need not stall mutation, but merely reduce the impact of deleterious mutations by encouraging heterozygosity.

    Lets take a common human example: syckle-cell anemia.

    Syckle-Cell is a mutation in the blood cells which causes them to be deformed and clog capillaries (amoung other things). The condition is fatal without treatment. However, having sycle-cell anemia also makes one resistant to malaria. How is this helpful?

    If someone has only one gene for syckle-cell (they are heterozygous recessive), they are resistant to malaria but the anemia wont kill them. If they have both bad genes (they are homozygous recessive), they die of the anemia. If they are homozygous dominant (both functional genes), they die of malaria. In malaria hot-zones, you get a lot of heterozygous recessive individuals and a lot of children dying of one condition or the other.

    Now, imagine that you had a mechanism to correct a deleterous mutation, but *only* if the mutation is homozygous. A homozygous dominant individual dies of malaria. A heterozygous recessive individual is mildly affected by the anemia but is protected from malaria. A homozygous recessive individual is *corrected to heterozygous* and is thereby protected from malaria without dying of anemia! You have a fourth of affected children dying instead of half.

    Plants may use this to end up with a stable heterozygous population for deleterious mutations which have some benefit, say a root hair deformation which nevertheless protects from parasites. This can actually speed up genetic drift by preserving mutations which might otherwise die out. In the malaria example above, it is common for human populations to quickly lose the gene if the malaria threat is removed. In the case where a corrective mechanism exists, the anemia would not be as harmful and might stay in the population longer (for the next outbreak).

    Not only does this not invalidate current ideas of evolution, it is obvious how a critter with such a mechanism would quickly have an advantage.
  • by Anonymous Coward on Wednesday March 23, 2005 @06:46PM (#12029556)
    Funny how this story only quotes Dr. (Bob) Pruitt. Most of this work was done by the first author Dr. (Susan) Lolle.

    Sigh. Pruitt is last author. In the bio-sciences, this means that he's the principle investigator - the guy with the lab, the guy with the money, the boss, the big cheese. More to the point, he's listed on the Nature paper as the contact person. You know, the person to talk to if you're wrighting a story? There are *plenty* of PI's who are female - if something happens in their lab, they're the ones who get to talk to the press.

    All of the comments in the NYT writeup are from male scientists.

    That's because you get quotes from the authorities in the field - those people who have the most experience. The ones with 20-30 years of experience. The ones who got their Ph.D. in the 70's or before. When there wasn't a lot of female graduate students.

    Your complaints are like saying that the CEO of a company shouldn't be quoted in news stories because all of the work to make the company sucessful is performed by others.
  • by WillAffleckUW ( 858324 ) on Wednesday March 23, 2005 @06:54PM (#12029676) Homepage Journal
    Not all genes are in the chromosomes, sometimes they're in Plasmids, especially with plants - or in humans, some of your DNA isn't in your chromosomes, they're in your Mitochondrial structures, hence you inherit them from your mother.

    However, a good controlled experiment should be able to rule this out, and I'm sure we'll all be talking about this in Biochem labs here at the UW this week.
  • by Zouden ( 232738 ) on Wednesday March 23, 2005 @06:59PM (#12029733)
    ...but how is this any different from a gene that's turned on or off?

    From the article:
    A mutated gene can be put right by various mechanisms that are already known, but all require a correct copy of the gene to be available to serve as the template. The Purdue team scanned the DNA of the entire arabidopsis genome for a second, cryptic copy of the hothead gene but could find none.

    They then go on to say they suspect RNA of holding the backup copy somehow. But (as the article mentions) RNA is unstable and unsuitable for holding data for any decent amount of time.
    IANAB (I will be one soon), but I suspect there is something they overlooked. For instance, when they 'scanned the genome', they probably scanned the online version (database). If they sequenced the genome of their particular plant, they'll find a backup copy.
  • by Anonymous Coward on Wednesday March 23, 2005 @07:08PM (#12029835)
    Look up "Null Hypothesis" in your nearest statistics textbook.
    Not to mention a quick lookup of Occam's Razor.
  • by harvardian ( 140312 ) on Wednesday March 23, 2005 @07:20PM (#12029946)
    Your explanation is fairly on the mark, and I'd mod it up except that I want to participate in the discussion.

    The thing that's so remarkable about this case is as you said: BOTH alleles of the gene of the plant were defective as inherited from their parents, and yet they somehow reverted to an allele from the grandparents, across the entire organism. According to current theory, sexual replication causes a kid to inherit one allele of each gene from each parent (and by "theory", I mean you can watch this happen under a microscope). If both alleles received are "faulty" (which is a sticky term to use in many cases), there's no known way for a newly fertilized cell to know this. There's no information about what the correct gene should look like except the two copies of the gene it has. In cancer, as you point out to address the parent post, there is always a source of information used to correct the mutation.

    In the case of UV damage, information exists in the form of two fused thimidine molecules (two T's). If a cell sees two fused T's, it has a repair mechanism for correcting them. But, importantly, if this mistake is not corrected before DNA duplication occurs, then random bases are paired with the T's, because they're damaged. Once this happens, each daughter cell has lost the information required to correct the problem, and the mutation persists. If this happens in an unlucky spot, you can get melanoma.

    In the case of other more serious damage, like double-stranded breaks, your cell pulls in the other copy of your genes and edits against that. The information needed for repair is the "good" copy of the allele in the sister chromosome.

    So you can see why this is so confusing -- in the case in the article the daughter cells, with two bad alleles for the gene they studied, are supposed to have no information pointing them to the gene from the grandparents. And yet they did, since they were able to fix it. The article postulates that this could be because a THIRD copy of the gene exists as RNA that's passed down from the grandparents (third since there are two chromosomes, each with a copy of the gene). If this were true, then the RNA would be the source of information required to fix the problem. Alternatively, there could be a specific protein that hunts down mutations in this gene and somehow fixes it, since it somehow bonds only to the correct version of the gene. But that's just my wild speculation.
  • by Artifakt ( 700173 ) on Wednesday March 23, 2005 @07:26PM (#12030007)
    A lot of genetically modified plants will be selected against where they escape into the wild. Golden Rice, for example, uses a lot of energy making Beta Carotine, that is, (from the plant's view), wasted. When its seeds get cross fertilized by wild rices the genes tend to be weeded out in the wild areas quite rapidly. Rice has generations lasting a year or less, and it's been estimated that the genes are 99% gone within 10 years. Even in cultivation, farmers have to suplement their seed stock saved from the last harvest with new purchases of fresh Golden Rice every few years to keep the yields up.
    That's not mutation as you've described, it's natural and artificial selection, but so long as there are unmodifed plants in the same areas as the GE ones, it tends to work that way, as the vast majority of GE features are disadvantagious under natural selection, and a lot of them are so disadvantagious they require real rigor to preserve via artificial selection. They're like Pekinese dogs in the wild.
  • by WillAffleckUW ( 858324 ) on Wednesday March 23, 2005 @07:47PM (#12030236) Homepage Journal
    The prior article on the research they did on this is at PubMed Article [nih.gov], or you can look up the current article at PubMed [nih.gov] yourself.
  • by cscoreo ( 860824 ) on Wednesday March 23, 2005 @07:48PM (#12030242)
    It's been known for decades that baker's yeast have the ability to fix mutated sex determining genes via exchange with an intact "cryptic" copy. The mechanism has been worked out in extreme detail. I don't think anyone ever thought they were the only organism that could do this . . . I guess it's nice to have proof, though.
  • by jezmund ( 102188 ) on Wednesday March 23, 2005 @09:19PM (#12031085) Homepage
    The explanation for this is pretty simple, and is pretty much standard practice whether you are male, female, or other. The order in which the authors are listed (in most scientific journals, at least) is a standard heirarchy. The author listed first contributed "the most" to the paper in terms of the research. To my knowledge, this generally also means this person wrote the paper. Authors listed after the primary author are understood to have contributed less to the paper. The final author listed is special, however. By convention, this author is the "owner" of the lab the research was performed in. In other words, Robert Pruitt is Susan Lolle's boss. So he gets asked all the questions because he's the most important person in the lab. Also (as noted in another comment) he likely doesn't do much research and spends much of his time shmoozing with reporters, writing grants, reviewing papers, and supervising the various different projects which may be running in his lab at any one time.
  • Re:Order of credit (Score:2, Informative)

    by espressojim ( 224775 ) <eris@NOsPam.tarogue.net> on Wednesday March 23, 2005 @09:42PM (#12031307)
    Hey yeah! That reminds me, I'll be submitting work to nature soon (in the next month), and since I'm not 1,2,4,5, I'm still somehow going to be first author.

    Oh wait, I wrote all the analysis code. Weeee. I guess I qualify for "going to the meetings."

    Seriously, I don't think all labs work that way. You'll have the PI get the last spot on the paper, and usually the person who did the most work get one of the first spots. Unless you work with a bunch of credit stealing a-holes, then it's time to work somewhere else.
  • by Anonymous Coward on Thursday March 24, 2005 @12:40AM (#12032549)
    Grabbed this URL from the RSS feed which naturally bypasses the NYTimes requirement to devulge your personal information. Not sure why they keep posting links to NYTimes without finding the pain-free links that are in the RSS feeds.

    http://www.nytimes.com/2005/03/23/science/23gene .h tml?ex=1269234000&en=00306bf37c75a71b&ei=5088&part ner=rssnyt
  • Re:Planet RAID. (Score:2, Informative)

    by shellsiebell ( 870701 ) on Friday March 25, 2005 @04:59AM (#12044396)
    Just to clear up any potential confusion, tRNA is not involved in sexual reproduction; that's just plain old DNA. tRNA is involved in protein synthesis. But for the record, plants use tRNA for protein synthesis in almost exactly the same way that animals do, and they do it using ribosomes closely analagous to animal ribosomes.

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