2004 Midwest Worm Meeting abstract 6
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Caenorhabditis elegans hermaphrodites display an age-related decline in fertility. Self-fertilized hermaphrodites display a sharp decrease in progeny production around day six of adulthood. This is caused by a depletion of sperm, since mated hermaphrodites that have an abundance of sperm produce progeny for several additional days. However, mated hermaphrodites display a sharp decrease in progeny production around day nine of adulthood, indicating that hermaphrodites undergo reproductive senescence despite ample sperm availability. We are using two approaches to analyze reproductive senescence. First, we have initiated F2 clonal screens to identify mutations that delay reproductive senescence. For one screening approach hermaphrodites were mated early in adulthood and then screened for greater than wild type progeny production on day nine and beyond. One candidate mutation was identified, am117, that caused hermaphrodites to produce ten times more progeny day nine and beyond and produce progeny for a greater length of time than wild type hermaphrodites when mated early in adulthood. am117 mutants also produced significantly more progeny when mated on day nine of adulthood, appeared to be smaller in size and had a small increase in lifespan in comparison to wild type. Furthermore, we analyzed existing mutant strains for changes in reproductive senescence. Mutations that cause an increase in hermaphrodite lifespan had various effects on hermaphrodite fertility later in life. Pharmacological agents that have been found to increase longevity in our lab also increased progeny production late in life for N2 hermaphrodites when raised on media containing the drugs. Second, we are trying to identify morphological and molecular markers that correlate with reproductive senescence in C.elegans hermaphrodites. These markers will assist in the identification and analysis of mutations that delay reproductive senescence. The markers may suggest the cause of the observed functional decline. By characterizing markers of reproductive senescence in C. elegans hermaphrodites and identifying mutations that delay this process the genetic and physical mechanisms that have evolved to control this process may be elucidated.