Quaglia, K. A. | Search bioRxiv

bioRxiv2026

Intermediate induction of germline apoptosis maintains fertility and progeny fitness during temperature stress

Organisms must be able to maintain the ability to produce high quality offspring despite experiencing stressful conditions. It is unknown how C. elegans maintain the ability to produce offspring during moderate temperature stress just below the range of temperature that cause sterility. We evaluated apoptosis, fertility, and several progeny fitness metrics in no-apoptosis, high-apoptosis mutants, and in wild strains that varied in their fertility level during moderate temperature stress to understand if apoptosis is a strategy C. elegans use to maintain the ability to produce offspring during a moderate temperature stress. We found that apoptosis mutants were less fertile with less fit progeny compared to wild type under a moderate temperature stress. Wild strains isolated from the environment showed variability in the increase in apoptosis, levels of fertility, and measurements of progeny fitness observed. We also found that an intermediate induction of apoptosis trended with higher fertility and progeny fitness in wild strains under a moderate temperature tress. These results suggest that apoptosis within an optimal range in the C. elegans germline is a strategy used to maintain the ability to produce high quality offspring despite experiencing a moderate temperature stress. Many species also have germline apoptosis, so apoptosis may be a strategy other species use to maintain their own fertility when experiencing stress conditions

cell biology↗

bioRxiv2024

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

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.

genetics↗