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Reproductive Signals Affect Lifespan In Roundworm C. Elegans, Offering Possible Insight Into Human Aging Process

Researchers at UC San Francisco have determined that signals from the reproductive system influence the lifespan of the nematode roundworm C. elegans, a phenomenon that could offer insight into the impact of reproductive development on aging in humans.

In the May 27 issue of Nature, they report that signals from germ cells - the sperm and egg in humans - shorten lifespan, while signals from the somatic gonads - the part of the reproductive tissue that surrounds the germ cells - lengthen lifespan, sending equal but opposite signals.

If the cells that give rise to the germ line are removed, the animals remain youthful longer, and live much longer than normal. And the explanation is not due to the failure of the animals to produce progeny - which researchers have speculated causes wear on the body, and thus aging - because animals that fail to have progeny for other reasons age normally.

Instead, the lifespan of the animal appears to be sensitive to the balance between signals from the germ line and somatic tissue. The authors speculate that this system allows the animal to coordinate its rate of aging with the development of its reproductive system, so that it produces progeny when it is still youthful.

The authors also report in the Nature paper that the reproductive signals act by modulating the activity of two genes - DAF-16 and DAF-2 - in a hormone signaling pathway whose components resemble those of the insulin and IGF-1 hormone systems in humans. The researchers previously discovered that these genes regulate aging in C. elegans.

As the pathway closely resembles the insulin/IGF pathways in humans, researchers suspect that lifespan may be regulated in a similar way in higher organisms, including humans. (Many basic biological processes, such as cell growth and tissue formation, are known to occur similarly in nematodes and humans.) The signals identified in the microscopic nematode have not been characterized, but the researchers
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Contact: Jennifer O'Brien
jobrien@pubaff.ucsf.edu
415-476-2557
University of California - San Francisco
26-May-1999


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