| Abstract |
As modest increases in temperature become more common due to global climate change, organisms are being subjected to moderate temperature stresses that can disproportionally affect fertility. Species that can buffer fluctuations in temperature through tissue or cellular responses in the germ line will therefore be more likely to survive moderate temperature stresses. Currently, what mechanisms are used in the germ line to facilitate maintenance of fertility under moderate temperature stress remain unknown. To address this, we investigated how germline apoptosis is modulated in Caenorhabditis elegans nematodes in response to moderate temperature stress. We found that wild-type animals increase their germline apoptosis levels from the physiological baseline in response to the moderate temperature stress. This induction of germline apoptosis was dependent on known and novel regulators of germline apoptosis including members of the conserved DREAM (Dp, Retinoblastoma (Rb)-like, E2F, MuvB) complex: LIN-35/pRB, LIN-54, and LIN-37, and proteins that regulate the synapsis checkpoint, BUB-3 and PCH-2. Additionally, repression of CED-9 function, the C. elegans Bcl2 ortholog, was necessary for full induction of apoptosis during moderate temperature stress. Finally, we found that changes in cytoplasmic streaming are correlated with changes to oocyte provisioning in wild-type animals but not mutants. Together, these data suggest an expanded role for LIN-35, the MuvB core of the DREAM complex, CED-9, and the synapsis checkpoint in maintaining fertility by activating apoptosis during moderate temperature stress.
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