Study Suggests Genome Instability Hotspots 72
Dr. Eggman writes "Ars Technica reports on a new study that suggests not only that certain areas of the mouse genome undergo more changes, but that changes to those areas are more tolerable by the organism than changes in other areas. Recently published in Nature Genetics, the study examined the certain copy number variations of the C57Bl/6 strain in mice that have been diverging for less than 1,000 generations. The results were a surprising number of variations. While the study does not address it, Ars Technica goes on to recount suggestions that genomes evolved to the point where they work well with evolution."
The Next Step (Score:5, Interesting)
I think a fascinating next step would be to see if, statistically speaking, viruses and transposons were channeled into jumping into these "safer to change" hotspots rather than other, more fragile areas of the genome.
It would seem to make some sense, given all the potential for genomic havok inherent in viruses and transposons' tendency toward hopping into the middle of genes.
That's a bit over-interpreted, IMHO (Score:5, Interesting)
What this really says is that the genome became, more or less, fault-tolerant. The ability to evolve really came out of that.
For starters, there is no part of the genome or ribosomes or whatever that actually produces mutations. On the contrary, most of the complexity in your cells is to prevent mutations, to the best of possibilities. It's the only way to have a coherent organism made of gazillions of cells. You don't want a cell in your palm to think it's supposed to grow into a nose, for example. And you really don't want cells to just start divided uncontrolled.
And you or the mouse have layers upon layers of defenses against that. The very reason why we're DNA based instead of RNA is to allow repairing single-strand mutations. But it goes on from there.
The very fact that you age is, pretty much, a defense against cancer: cells have a maximum division number counter, based on what tumor size still likely wouldn't kill you. (Hence also why larger species tend to live longer: they get a bigger limit there.) When more and more cells have reached that limit, then more and more damage can't be repaired, and you discover the fun of old age. And then you die.
Etc.
At any rate, the major thing is: there is no part in the genome that says you should evolve. Read: mutate. It actually tries to prevent mutations, hence evolution.
But mutations happen anyway, and some will happen in the sperm or eggs, or the first stages of embryo formation. You can't 100% prevent those. They _will_ happen. And the choices from there are basically two: either the result can still live with that mutation, or it dies.
Hence what they discovered here: natural selection favours the kind of genome that can tolerate mutations when they happen anyway. A species where the slightest change results in death will be at a disadvantage, compared to a species where more individuals survive even with mutations.
Sure, in the long term that also means being to evolve and cope with environment changes. No doubt. But I think there's a far stronger short-term pressure to achieve the same result. And most likely that's really what we're seeing there.
Re:That's a bit over-interpreted, IMHO (Score:3, Interesting)
That's true more or less by definition, but I think you're overlooking something simple. A more complex organism has more opportunities for nonfatal mutations. That is, Mycoplasm genitalium, probably the simplest known bacterium, is extremely vulnerable to deleterious mutations. If it loses a gene that codes for a vital self-component, odds are it hasn't got a backup process for that component--it's dead. Whereas a more metabolically complex bacterium may have multiple pathways that produce necessary components. So it's not surprising that when we look at complex genomes, we see the capability to withstand mutation.
So greater complexity (more genome) means more opportunity for mutation, but also more redundacy and failure tolerance. So it's no surprise that
Re:Maybe organisms with DANGEROUS changes are DEAD (Score:2, Interesting)
Re:That's a bit over-interpreted, IMHO (Score:3, Interesting)
The shortening of telemeres with age does indeed protect against cancer although the link between the length of a telemere is a dubious test of longevity. some small rodents for example, lengthen their telemeres because the gene that produces telemerase doesn't switch off in early development like a lot of other species. They don't live that long, not because of the length of their telemeres, but because of other factors. Consider this: suppose there were a vastly more efficient genetic repair enzyme that caused bacteria to be far less likely to mutate. Would this enzyme give an overall advantage [preventing deleterious mutations] over the current genetic repair enzymes [good but not perfect] in the case of antibiotics? In that case, a lack of genetic change is a disadvantage.