Forgot your password?
typodupeerror
Biotech Science

Flatworms Defy Aging Through Cell Division Tricks 106

Posted by Unknown Lamer
from the ail-hail-the-immortal-flatworm dept.
An anonymous reader writes "Researchers from The University of Nottingham have demonstrated how a species of flatworm overcomes the aging process to be potentially immortal. The discovery, published (abstract; full text PDF) in the Proceedings of the National Academy of Sciences, is part of a project funded by the Biotechnology and Biological Sciences Research Council and Medical Research Council and may shed light on the possibilities of alleviating aging and age-related characteristics in human cells." After finding the gene for telomerase synthesis in the worms, the researchers were able to observe that the worms "...dramatically increase the activity of this gene when they regenerate, allowing stem cells to maintain their telomeres as they divide to replace missing tissues."
This discussion has been archived. No new comments can be posted.

Flatworms Defy Aging Through Cell Division Tricks

Comments Filter:
  • Trade off (Score:2, Interesting)

    by funtapaz (1406785)
    I wonder what they sacrifice for this? I'm guessing they are highly prone to cancer or something. I'm nature I doubt they live long enough for problems like that to manifest.
    • by Culture20 (968837) on Tuesday February 28, 2012 @01:16AM (#39182279)
      The trade off? They're highly prone to being a flatworm.
    • Re:Trade off (Score:5, Informative)

      by izomiac (815208) on Tuesday February 28, 2012 @02:34AM (#39182551) Homepage
      In humans, telomeres limit cells to ~50 divisions, which is probably related to how DNA replication is only 99.9998% accurate. After that many divisions, the genome is 0.001% different from when it started, which is one error per 10,000 base pairs, or an error in 1/3 of all genes. This is in addition to the slow rate of spontaneous mutations you accumulate over your lifetime.

      In general, fatal mutations don't matter, the stem cell will just divide again (or be dead), and cells are specialized so only a small number of genes are relevant. Furthermore, cells work together, so if two nearby cells have different lineages then they have different errors, and can likely compensate for each other. Still, you don't want too many errors in your cell replication control genes (i.e. protooncogenes ==> cancer), nor can cells function well with a tremendous number of errors (i.e. "aging"). Telomeres also help divvy-up the workload among stem cells so the most eager doesn't monopolize the work.

      For flatworms, all this likely entails a fast mutation rate. So what if 90% of its offspring die? The one that takes hold in a new host can produce thousands of offspring, and quickly changing their immunologic profile increases the odds of that.
      • Re:Trade off (Score:4, Interesting)

        by Zorpheus (857617) on Tuesday February 28, 2012 @07:54AM (#39183721)
        Very interesting. I am wondering now how Humans survive for more than 50 generations, since gametes are also fomred by cell division.
        • Re: (Score:3, Informative)

          by Anonymous Coward

          telomerase - it's just restricted to the germ line

        • by Boronx (228853)

          Miscarriage, I reckon.

        • by izomiac (815208)
          Offspring for each generation are subjected to natural selection, which can be thought of as an independent correcting factor in this case. A sperm or egg with detrimental mutations won't ever reach its counterpart. Most people are familiar with how many millions of sperm don't make it, but for eggs each woman has ~400,000 and only ~400 of those activate (the healthiest tend to do so earlier in life). At least 25% of fertilized eggs self-abort in the first trimester. From there, the number of fetuses th
      • by Anonymous Coward

        Note that not all flat worms are parasitic, e.g. Planaria sp.

      • It's worth adding that even in humans, telomerase (which is produced naturally by cells) can regrow damaged telomeres. The implications and reasons for this are not yet clear, but it's been known since the 1980s at least
      • Re:Trade off (Score:4, Informative)

        by tOaOMiB (847361) on Tuesday February 28, 2012 @01:31PM (#39186633)

        In humans, telomeres limit cells to ~50 divisions, which is probably related to how DNA replication is only 99.9998% accurate. After that many divisions, the genome is 0.001% different from when it started, which is one error per 10,000 base pairs, or an error in 1/3 of all genes. This is in addition to the slow rate of spontaneous mutations you accumulate over your lifetime.

        Where did you get your numbers? Human DNA replication (in normal cells with no damage) is 99.99999999% accurate (i.e. about 1 mutation per 10^-10 base pairs). Please do not mod parent informative for this misinformative post!

        • by izomiac (815208)
          Sorry, it appears the rate was revised the year I graduated, so I was using older information (1 per 600,000). I will admit that one error per three genes from replication alone did seem too high to me. In vivo error rates seem to be one per 10^9 base pairs [nature.com]. Given that it's a review article, I'd have to do a lot of reading to determine how DNA packing and such affect that rate (or how they measured in vivo rates rather that ideal in vitro).

          That rate would only allow for 150 mutations per cell before h
          • by tOaOMiB (847361)
            Environmentally-induced mutation definitely does play a large role in tumor formation--that's why smoker's get lung cancer, sunburns can lead to skin cancer, etc! There's also viruses that can play a role.

            However, we also don't really know how many mutations are necessary for cancer to arise, and one of the first things to happen may be either immortalization through mechanisms including telomerase activity (or the tumor could arise in stem cells where this activity is already present) or (more often) a
            • by izomiac (815208)
              The number is about eight for common cancers. Generally you need about three or so before the mutation rate increases dramatically. Still, that works out to about a one in ten thousand chance of getting those three mutations in a cell, in highly active cells (~30 divisions) which are fairly rare in end-organ tissue where cancers arise. While the human body has ~10 trillion cells, 90% of those are symbiotic bacteria, and breast/prostate/lung tissue isn't very dense. From there, the immune system kills th
      • by mhajicek (1582795)
        So what's needed is a RAID controller for DNA, that will sample code from several cells and derive the original code, then undo any mutations. Suppose that's within the realm of possibility?
      • by jbengt (874751)
        If 50 cell divisions created errors in 1/3 of all genes, then life would be doomed before 50 generations pass, since the germs cells also must replicate, at least once per generation. Also, just to clarify, telomerase is not a gene, it is a repeating stretch of DNA that ends the chromsome, like the plastic tip of shoelaces that keeps them from fraying. I have no clue how telomeres could possibly "divvy-up the workload" as the parent says.
        • by izomiac (815208)
          If cells could divide 50 times without their less fit offspring dying, a single bacterium could produce one kilogram of offspring in about a day. For perspective, in two more days its offspring would weigh much more than the Earth. Plus, most mutations are silent, or inconsequential, such as the ones that make-up your fingerprint.

          Telomerase is a protein. It has a gene, but it's not a repeating segment (the promoter/enhancer might be, but that's not what you mean). Telomeres are repeating segments tha
    • by c0lo (1497653)

      I wonder what they sacrifice for this? I'm guessing they are highly prone to cancer or something.

      Cancer most likely: Hayflick limit [wikipedia.org].

      • by Anonymous Coward

        I wonder how this would affect naked mole rats; we've never observed cancer in them or been able to give them cancer. Flatworm + mole rat == immortality?

    • by Daetrin (576516)
      I believe there have already been very limited tests of telomerase in humans, but one of the big fears is indeed that it will increase the odds of cancer. It'll be interesting to see what happens when (if?) we have cures for most kinds of cancer.
    • "I doubt they live long enough for problems like that to manifest."

      If you train a flatworm to pass a labyrinth and then cut the flatworm into pieces, each piece will remember the labyrinth!

      So, with this memory they don't need to live much longer, piecewise.

      They have all the nice tricks up their sleeves. The trade-off may be their looks.

      • by Boronx (228853)

        Not only that, but if you feed trained worm to an untrained one, it'll know the labyrinth.

    • Now you are making a common mistake of assuming of intelligent design, you may not actually subscribe to that thought but you are not really following evolutionary theory when you assume that an advantage needs a trade off.

      The intelligent design (NOT CREATIONISM) approach assumes that there is a plan or a benefit to every evolutionary change. While evolution is more based on pure random events where a random mutation can either give the life form an advantage where it could have offspring, or it could hind
      • by funtapaz (1406785)
        I'm definitely not one who follows ID. It just seems like there's usually some sort of disadvantage to being "immortal." That disadvantage usually seems to involve cancer because telomerase seems to be useful in the prevention of cancer. I don't know enough to speak beyond that though.
  • A flatworm only has, maybe, a few hundred brain cells, but if they get regenerated are they a "copy", or just "new"?
  • Disturbing (Score:5, Funny)

    by Dan East (318230) on Tuesday February 28, 2012 @02:18AM (#39182495) Homepage Journal

    I find it disturbing that my tapeworms will outlive me.

  • by Anonymous Coward on Tuesday February 28, 2012 @02:32AM (#39182545)

    Here is a video from the researchers themselves.
    http://www.test-tube.org.uk/videos/pages_aziz_immortal_worms.htm

    • According to the guy, raw sewage dumps directly into the nearby river -- seriously? He says, "There's where a lot of crap comes out of hospital."
  • Obligatory (Score:2, Funny)

    by tonique (1176513)
    I, for one, welcome our new flatworm genes carrying overlords.
  • by Anonymous Coward

    They've found the Flatworm of Youth!

  • for ( i = 1; welcome( our ); ) new Imortal::FlatwormOverlords;
  • by dtmos (447842) * on Tuesday February 28, 2012 @06:44AM (#39183475)

    From the Discussion section of the linked paper:

    We find that in the model species S. mediterranea, asexual animals demonstrate the potential to maintain telomere length during regeneration. Sexual animals appear to only lengthen their telomeres through the sexual reproduction process. This finding suggests that asexual individuals will be able to avoid senescence over evolutionary timescales using telomerase, a prerequisite for the formation of an evolutionarily stable fissionating asexual lineage. [. . .] The difference we observe between asexual and sexual animals is surprising, given that sexual animals also appear to have an indefinite regenerative capacity. We conclude that either they would eventually show effects of telomere shortening or that they are able to use another chromosome end-maintenance mechanism not involving telomerase. [emphasis added.]

    So both sexual and asexual animals seem to have an indefinite regenerative capacity, but sexual animals appear not to lengthen their telomeres except through the sexual reproduction process. So how do the sexual animals attain their indefinite regenerative capacity, and why does the mechanism seem to be different from that of the asexual animals? I guess the next experiment is to start slicing up sexual animals.

    • by hardie (716254)

      I was interested in this too. Not that I read the actual paper, but why do they think telomerase is the cause of longer life in the asexual worms? Aren't the sexual worms a counterexample?

    • by mcgrew (92797) *

      Asimov, a biochemist, whote a short SF story about this very thing: Playboy and the Slime Gods [wikipedia.org]. The wiki article is incomplete, Asimov explained his motivations is reprints in various of his books.

  • What, still no references to the film "In Time"?
  • Now when this will be made available to humans the whole game will change again: Basically the corporate overlords will live forever and they will only have to change the workers generation by generation. This until they will create enough robots to do the job instead of the workers. Then most of the humanity will be kinda obsolete. They will live in closed premises, served by robots, having fun among them. the rest of us will freely participate in madmax
  • by cribera (2560179) on Tuesday February 28, 2012 @09:48AM (#39184319)
    The Immortal Life Cycle of Turritopsis, with diagrams http://9e.devbio.com/preview_article.php?ch=2&id=6 [devbio.com] __ Inmmortal human cells. http://www.smithsonianmag.com/science-nature/Henrietta-Lacks-Immortal-Cells.html [smithsonianmag.com]
  • It isn't clear at this point if the telomere hypothesis works at a cross-species level. In some species, telomere length is apparently not correlated with aging. In particular, there are some birds which have short telomeres but long lifespans. There's a very good book aimed at laypeople on the science of understanding of aging and the history of attempts- "The Youth Pill" by David Stipp. The only minor disclaimer is that the field is changing so fast that the book is already slightly out of date. But it co
  • ... and all those flatworm dudes will be picking up hot flatworm babes long into their old age.

  • I wonder if there could be some advantages to mortality. It just seems it would be easier (take less energy) to keep an existing organism in good repair indefinitely, compared to starting over with a new generation. If so, then lifespans evolved to be deliberately shorter than need be. If a tree can live 5000 years, why not an animal?

    Shorter generations allow faster adaptation and evolution. Maybe immortality makes organisms so risk adverse that it becomes detrimental to the survival of the species.

  • I wish I had known this years ago when we were writing and printing The Evil Platy-hell-minthes, Planaria of Destruction comics. Then more megalomanicial rants about the benefits of immortality could have been included and they would have had a good grounding in biology instead of Pullingitoutofmyassology.

  • by nohelix (1244378) on Tuesday February 28, 2012 @01:13PM (#39186443)
    The planarian has come up several time here on /. and I thought that some people might like a quick intro these guys.

    The flatworm used in this study is the planarian S. mediterranea, a free living (i.e. non-parasitic) flatworm. They have a distinct head and tail. They have non-lensed eyes capable of detecting the direction and strength of light allowing them to move away from it. Finally, they have a bi-lobed cephalic ganglia (rudimentary brain) and a rudimentary CNS. A similar species of planarians (dorotocephala) is frequently seen in high school science class.

    There are 2 varieties of this species - one reproduces asexually while the other reproduces sexually. Both varieties are capable of complete regeneration (i.e. a full worm from almost any fragment) when cut. In both cases, the only dividing cells in the worms are stem cells called neoblasts.

    Fun Fact: Thomas Hunt Morgan did many of the initial experiments on planarians.

    -----
    Standard disclaimer: I work in a lab that uses these animal.
  • ...the benefit of mortality is that bad people always die. No matter how much power one sociopath picks up, we only have to tolerate them for a century. Let's not ruin a good thing by "fixing" that.

Make headway at work. Continue to let things deteriorate at home.

Working...