@article{1570,
  keywords = {Animals, Mutation, Signal Transduction, Female, Male, Aging, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Longevity, Reproduction, Transforming Growth Factor beta, Body Size, Diet, Ovulation, Spermatozoa},
  author = {Shijing Luo and Wendy Shaw and Jasmine Ashraf and Coleen Murphy},
  title = {TGF-beta Sma/Mab signaling mutations uncouple reproductive aging from somatic aging.},
  abstract = {<p>Female reproductive cessation is one of the earliest age-related declines humans experience, occurring in mid-adulthood. Similarly, Caenorhabditis elegans{\textquoteright} reproductive span is short relative to its total life span, with reproduction ceasing about a third into its 15-20 day adulthood. All of the known mutations and treatments that extend C. elegans{\textquoteright} reproductive period also regulate longevity, suggesting that reproductive span is normally linked to life span. C. elegans has two canonical TGF-beta signaling pathways. We recently found that the TGF-beta Dauer pathway regulates longevity through the Insulin/IGF-1 Signaling (IIS) pathway; here we show that this pathway has a moderate effect on reproductive span. By contrast, TGF-beta Sma/Mab signaling mutants exhibit a substantially extended reproductive period, more than doubling reproductive span in some cases. Sma/Mab mutations extend reproductive span disproportionately to life span and act independently of known regulators of somatic aging, such as Insulin/IGF-1 Signaling and Dietary Restriction. This is the first discovery of a pathway that regulates reproductive span independently of longevity and the first identification of the TGF-beta Sma/Mab pathway as a regulator of reproductive aging. Our results suggest that longevity and reproductive span regulation can be uncoupled, although they appear to normally be linked through regulatory pathways.</p>},
  year = {2009},
  journal = {PLoS Genet},
  volume = {5},
  pages = {e1000789},
  month = {12/2009},
  language = {eng},
}