Abstract
Lifespan is shortened by mating, but these deleterious effects must be delayed long enough for successful reproduction. Susceptibility to brief mating-induced death is caused by the loss of protection upon self-sperm depletion. Self-sperm maintains the expression of a DAF-2 insulin-like antagonist, INS-37, which promotes the nuclear localization of intestinal HLH-30/TFEB, a key pro-longevity regulator. Mating induces the agonist INS-8, promoting HLH-30 nuclear exit and subsequent death. In opposition to the protective role of HLH-30 and DAF-16/FOXO, TOR/LET-363 and the IIS-regulated Zn-finger transcription factor PQM-1 promote seminal-fluid-induced killing. Self-sperm maintenance of nuclear HLH-30/TFEB allows hermaphrodites to resist mating-induced death until self-sperm are exhausted, increasing the chances that mothers will survive through reproduction. Mothers combat males' hijacking of their IIS pathway by expressing an insulin antagonist that keeps her healthy through the activity of pro-longevity factors, as long as she has her own sperm to utilize.
Highlights
The battle between the sexes is played out across the animal kingdom: males compete with one another to pass on their own genomes, often at the expense of female health, and females, in turn, must devise strategies to reduce the deleterious effects of mating in order to successfully complete reproduction
We previously showed that Insulin-IGF-1 signaling (IIS) mediates seminal fluid-induced killing by inducing DAF-16/FOXO nuclear exit (Shi and Murphy, 2014)
(Rosenquist and Kimble, 1988) are protected from brief mating-induced death for a longer period of their lifespan than wild-type hermaphrodites (Booth et al, 2019), and we found that the HLH-30 binding motif is enriched in promoters of genes that are up-regulated in (fem-3(q20)) hermaphrodites compared to animals with normal levels of sperm (Figure 3—figure supplement 1; Supplementary file 3)
Summary
The battle between the sexes is played out across the animal kingdom: males compete with one another to pass on their own genomes, often at the expense of female health, and females, in turn, must devise strategies to reduce the deleterious effects of mating in order to successfully complete reproduction. Sexual antagonism is evident in Caenorhabditis elegans, where signals from males kill hermaphrodites through three distinct mechanisms: germline activation (Shi and Murphy, 2014), seminal fluid transfer (Shi and Murphy, 2014), and, at high doses, male pheromone toxicity (Maures et al, 2014; Shi et al, 2017). While germline activation is necessary for reproduction and the resulting lifespan decrease is shared both across sexes and species, seminal fluid (SF) killing appears to be used for the purpose of ‘sperm competition’ (that is, competition between males) within the species: seminal fluid transfer induces death of mothers just after they have produced all of that male’s progeny, eliminating the possibility of the mother re-mating with a different male (Shi and Murphy, 2014). We noted previously that mating-induced death occurs only after C. elegans hermaphrodites produce all their progeny (Shi and Murphy, 2014); this delay is necessary for successful reproduction, but the
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