LIN-35 and the DREAM complex promote temperature stress induced increases in germline apoptosis and cytoplasmic streaming in C. elegans

Abstract

As modest increases in temperature become more common due to global climate change, species are being subjected to moderate temperature stress that can disproportionally affect species fertility. Species that can buffer fluctuations in temperature through tissue or cellular responses in the germline will therefore be more likely to survive moderate temperature stress. Currently, what mechanisms are used in the germline to facilitate maintenance of fertility under moderate temperature stress are unknown. To address this, we investigated how germline apoptosis is modulated in Caenorhabditis elegans nematodes in response to moderate temperature stress. We found that wildtype 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 conserved members of the DREAM complex, including LIN-35, the C. elegans homolog of the retinoblastoma tumor and members of the MuvB core, LIN-54 and LIN-37. We also found that LIN-35, LIN-54, and LIN-37 were necessary for DNA damage induced apoptosis. Additionally, induction of germline apoptosis during moderate temperature stress was dependent on repression CED-9 function, the C. elegans Bcl2 ortholog. Finally, we found that changes in cytoplasmic streaming likely lead to changes to oocyte provisioning in wildtype animals but not mutants. Together, these data suggest an expanded role for LIN-35, CED-9, and the DREAM complex in maintaining fertility by activating apoptosis during moderate temperature stress.