The final activating step in the Notch signaling pathway is the proteolytic cleavage that releases the intracellular receptor domain from its transmembrane domain tether. This cleavage is mediated by the gamma-secretase complex, whose four subunits have been shown to be essential for Notch signaling. The presenilin subunit contains the catalytic core of the enzyme complex, and many organisms contain two alternative forms of presenilins. In C. elegans, Notch signaling is mediated by the by SEL-12 and HOP-1 presenilins. For most known Notch signaling events, SEL-12 and HOP-1 function redundantly, such that Notch activation can be successfully mediated by either presenilin. The SEL-12 presenilin mediates at least one Notch signaling event for which HOP-1 is not available, or is otherwise not effective, because
sel-12 mutant hermaphrodites display a penetrant egg-laying defective phenotype that is similar to that of
lin-12 Notch hypomorphic mutants. In contrast, a unique role for the HOP-1 presenilin has not yet been demonstrated. We analyzed the null
hop-1(
ar179) phenotype and demonstrate a reduction in germ line output, as measured by self-brood size, mated brood size, and reproductive span. Normally, GLP-1 Notch signaling in the distal gonad is necessary to support germ cell proliferation during larval development as well as continuously during adulthood. In the absence of any presenilin function, germ cells prematurely enter meiosis without significant proliferation, resulting in a sterile animal. Since both
hop-1 and
sel-12 single mutants are fertile, a likely explanation for the reduced fecundity of
hop-1(
ar179) hermaphrodites is that HOP-1 and SEL-12 presenilins contribute additively to the total Notch signaling capacity of the gonad, such that both presenilins are always needed for maximum fecundity. Our investigation into the underlying cause of
hop-1(
ar179) reduced fecundity revealed a different explanation: First, we found that hermaphrodite oocyte production, but not sperm production, is compromised in
hop-1(
ar179) hermaphrodites. Second, we found that
hop-1(
ar179) animals begin adulthood with robust germ cell proliferation, but then fail to sustain proliferation through adulthood. We conclude that
hop-1(
ar179) animals have reduced fecundity because Notch signaling ceases in the adult gonad, generating a "delayed Notch phenotype." These results reveal an absolute requirement for HOP-1 function in adult gonads, where SEL-12 is likely unavailable. We are currently mapping the timing of the switch to HOP-1-dependence, and its ramifications on germ line maintenance in the adult.