One for the molecular biologists, I guess.
So, one of the main factors in ageing is the accumulation of errors in our DNA.
But somehow, gametes are protected from such damage, else we’d produce “aged” offspring (or, probably more likely: the embryo wouldn’t be viable).
How?
On the male side of things I can imagine cells with errors being eliminated, but what happens on the female side?
ETA: What I meant by “aged” offspring, was that over several generations errors would build up, not that the offspring would inherit all the effects of ageing from the parent.
On the female side, cell division is arrested in the gametes after they develop in utero until they “ripen” once a month after puberty. So there’s not continual division of the DNA in the gametes which would introduce errors. ETA: The ovum of a 50 year old woman will have divided exactly as many times as the ovum of a 19 year old woman.
As for the male side…uh…I got nothin’. They’re produced continuously from puberty on from (I would assume) cells which have been replicating all along.
Of course, conditions caused by genetic abnormalities are more common in babies with older parents, so maybe the premise of your question is flawed - maybe mature (or hypermature) adults do not produce identical offspring to young adults.
Not really. It’s one hypothesis, but we really don’t know what causes aging and there are many other hypothesis out there.
Granted, and if ageing is entirely caused by “programmed” causes, then the answer to the OP becomes pretty simple: gametes aren’t programmed to die / wear out.
But I think there is enough evidence of genetic damage in humans for us to believe that it is at least part of the cause of ageing. The so-called accelerated ageing diseases, for instance, are mostly caused by mutations affecting the DNA repair mechanism.
Cite? (The more “erroneous” gametes will not be viable anyway. That little sperm that was first to wriggle his way to his goal? He might have better genes than his Daddy!)
Evolution depends on mutations (“errors”) and some mutation rate might be considered optimal. Perhaps fewer “errors” in gametes would would give a less-than-optimal mutation rate.
What I’ve read is that telomere shortening is an important factor in aging: DNA can only be transcribed some finite number of times until the telomere is too short. But telomere shortening is not universal; there are mechanisms to expand the telomere section of DNA, including one, IIRC, used for gametes.
Lobsters, famously, do not age! (:eek: ) IIRC a mechanism to maintain long DNA telomeres is part of that.
This is actually a very interesting question, and is one reason why stem cell research is so important. There has to be some way for adult cells to create embryonic cells - obviously. How that works isn’t completely understood, and researching it should provide some very valuable discoveries.
Sperm cells have to compete against each other, and they have to negotiate a difficult path to even get to the ovum, and from memory it then still takes quite a lot of healthy sperm cells to get the ova in a receptive state. So even though the continuing generation of new sperm cells increases the chance of errors, at least with regards to sperm cells, there’s a lot of weeding out of less able copies.
Also, I’m not sure of the percentage, but not nearly all fertilizations result in a successful pregnancy so there’s a lot of weeding out of less adaptive zygotes and embryos too.
And of course, the resulting young still have to reach adulthood to be able to reproduce, which again selects for successful “grand kids”. One thing to keep in mind is that there is no platonic “ideal” human which needs to be copied exactly. Variation/mutation, if moderated by selection, is useful from a species point of view.
OK, hang on. Lobsters are immortal? :dubious:
Googles
Apparently so! :eek: Until they die from some external cause.
They also never stop growing. Could there be a lobster somewhere in the ocean the size of a dump truck and from the time of Caesar? :eek:
Screw eating lobsters. Now I just want to catch one and keep it around to see how many millennia it could last and huge it could get.
We’re gonna need a bigger hollandaise pan…
Well yes, but surely only a tiny minority of mutations, even if they are very deleterious to the body as a whole, will actually affect the motility, viability etc of a sperm cell. Sperm are not very complicated compared to whole bodies.
I thought that at least some of the accumulated mutations got weeded out during recombination. Isn’t that what meiosis and recombination are thought to be largely for?
[quote="Martian Bigfoot, post:9, topic:564719"]
OK, hang on. Lobsters are immortal? :dubious:
*Googles*
Apparently so! :eek: Until they die from some external cause.
[/QUOTE]
Lobsters, the elves of the Seventh Age! :D ([The Sixth Age is apparently thought to have ended with the downfall of Hitler](http://www.glyphweb.com/arda/f/fourthage.html).)Here are some of the ways. First, a woman is born with her full complement of eggs and is not making more. Yes, they can still mutate but I believe most mutations occur during cell division. For the males, it is a reasonable guess that among the millions of sperm produced during the average ejaculation, the healthiest have the best chance of fertilizing an egg. I seem to remember reading somewhere that something like 40% of sperm are obviously defective and cannot do whatever they do to get to an egg. Finally, many, I imagine most, non-viable fetuses are destroyed naturally and result in spontaneous abortions, often before the woman knows she is pregnant.
There may be other mechanisms, but these come to mind.