The stem cells stick around for life, so sperm generated by older men carry (More Mutations

http://sageke.sciencemag.org/cgi/content/citation/2003/31/nw108?ck=nck

Evolutionary Oxymoron. Sperm development encourages mutations that harm offspring. Mary Beckman.-------------------------------------------------------------------------------------



In the second phase, called the adult phase, SrAp divide asymmetrically to produce one SrAp and another cell whose descendants will ultimately produce sperm. In this phase, the number of SrAp remains constant. These cells divide every 16 d [18], so assuming this phase begins at puberty (age 13), donor 374 who is age 62 has experienced a = 1,127 adult phase generations, and donor 854 who is age 54 has experienced a = 943 adult phase generations. The total number of divisions in the testis in this phase is equal to (a × 2g). For these donors, there are approximately 500 (a × 2g/2g+1) more opportunities for replication-dependent mutation in the adult phase than in the growth phase, and because we assume identical mutation rates per cell division in both the growth and adult phases, there will also be, on average, this many more mutations in the adult phase. These mutations will be randomly spread throughout the testis. Unlike in the growth phase, mutations in the adult phase lead to only a single mutated SrAp (and approximately 25 other mutated germ cells [23]). If the testis mutation frequency is f, then f ÷ a is an upper bound for the mutation rate λ (this inequality ignores mutations in the growth phase).




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But the clusters of mutant cells could be explained if the mutant cells made copies of themselves more frequently than normal cells.

If a mutant cell divided into two copies of itself every four to five years, the extra copies would be enough to explain the clusters, the researchers said. They added that the model explains the increase in Apert risk with paternal age, while noting that other selection-based models also may be able to explain the same data.


"You would expect that when a new mutation arose, it could arise virtually anywhere in the organ," said Norman Arnheim, holder of the Ester Dornsife Chair in Biological Sciences at USC and one of the co-leaders of the project along with computational biologist Peter Calabrese.

"But when we divided the testes up, we didn't find that. What we found were some very big clusters of precursor cells that were mutant."