Princeton scientists have identified genes responsible for controlling reproductive life span in worms and found they may control genes regulating similar functions in humans.
The work suggests that someday researchers may be able to develop ways to maintain fertility in humans, allowing women who want to delay having children to preserve that capacity and extend their reproduction, and to prevent maternal age-related birth defects.
The research, led by Coleen Murphy, an assistant professor of molecular biology and the Lewis-Sigler Institute for Integrative Genomics, was published in the Oct. 15 edition of Cell.
"Could you give someone a drug or supplement when they are in their mid-30s that would keep their oocytes (immature egg cells) healthy? That's the goal," Murphy said. The approach, she said, would be similar to the regimen of daily allotments of folic acid taken by pregnant women to prevent the development of spina bifida in the fetus.
In humans, reproductive aging causes problems in the quality of the eggs produced about a decade before the egg supply runs out. This can lead to miscarriages and worries about chromosomal abnormalities. "In humans, this suggests that quality, not quantity, is the limiting factor," Murphy said. "The question was whether the same is true in worms. And the answer is yes."
"We have found that there are many shared genes between worms and humans in terms of their reproductive qualities," Murphy said. "So this isn't just about worms and how they reproduce."
In the study, the researchers sought to understand what happens in roundworms, C. elegans, as reproductive aging sets in. They compared the activity levels of genes in normal roundworms with those of mutant roundworms that produce eggs until old age. They found that a complex of genes important to human reproduction is more active in the second group. These genes affect the ability of eggs to be fertilized
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