So we have this here thread about cloning critters, and it is pointed out the DNA used to produce a clone is damaged (aged?) and thus produces an inferior critter. Presumably this has to do, in part at least, with worn telomeres on the chromosomes introducing premature age to the otherwise new critter. Sorta like making a new car out of old parts?
So…is there some point during meiosis where chromosomes are fitted with shiny new telomeres? Why are gametes made to OEM specs while other actively reproducing tissues copy damaged information? I suppose sperms & eggs are made from a relatively isolated stock and so are more closely related to the originals. Which is fine for eggses, but sperms are produced by the gazillions and still seem to be pretty accurate even as the body is falling apart.
Likely the answer is something along the lines of “Dude, you’re stupid and have a completely misguided understanding of biology.” And I probably don’t really know the question I’m asking. Thank you for your support.
Female humans, at least, are not born with all their eggs as is commonly believed. They are born with all their primary oocytes. (Oocyte is an excellent Scrabble word.) A primary oocyte is a proto-gamete that contains the complete set of chromosomes from the mother’s genetic code. During ovulation, the primary oocyte splits via meiosis, creating two secondary oocytes, each with one randomly-distributed half of every chromosome pair. Those are the eggs that get fertilized by a sperm cell, containing half the genetic material from the father.
The meiosis process doesn’t always work perfectly. In particular, older women are at greater risk of meiosis errors that cause certain trisomies, like trisomy 21 (Down syndrome.)
So while eggs don’t exactly age, the process that creates them is subject to certain errors which increase with age.
The chromosomes in the primary oocytes are arrested in prophase I of meiosis, where the homologs are being held together by cohesive linkages. There’s a series of protein circles that hold the chromosomes together, possibly like handcuffs. These proteins need to remain in place for up to forty years before ovulation moves meiosis onward. If the linkages fail for some reason, you can get nondisjunction of the chromosome, which is how you get Down syndrome and other defects.
There’s some evidence to suggest that it’s the weakening of these linkages that is at least partially responsible for the maternal age effect - the increase in risk of Down syndrome and other birth defects with maternal age.
As to the original OP question, eggs and sperm are made from germline stem cells - special cells that retain their “youthfulness” indefinitely. Telomerase is active in these cells to keep things tidy. Although I’ll also add that in my opinion, the importance of telomere shortening in the aging process has been somewhat overstated in the popular understanding. There are lots and lots of other things going on too.
Clearly, though, the normal kinds of cell replication shorten telomeres, while some other kind(s) must exist that does not (or we wouldn’t be here: each successive generation would have shorter telomeres.)
Can someone elaborate?
Do stem cells divide without shortening telomeres? Or is it only in the germ cell line?