Date of Award
Summer 2026
Document Type
Dissertation
Degree Name
Doctor of Philosophy (PhD)
Department
Biological Sciences
First Advisor
Lisa Petrella
Abstract
In organisms as diverse as flies, nematodes, and mammals, as temperature increases, fertility decreases. Many species, especially exothermic ones, are therefore especially susceptible to the impacts of increase surface temperatures due to global climate change. Thus, organisms likely have cellular mechanisms that buffer the effects of elevated temperatures to produce fit offspring despite experiencing temperature stress. However, such buffering mechanisms remain poorly understood. The goal of this dissertation is to investigate germline apoptosis as a temperature stress response mechanism in Caenorhabditis elegans to buffer fertility and progeny fitness during moderate temperature stress. First, we demonstrate that the presence of apoptosis during moderate temperature stress buffers fertility and progeny fitness. In worms that carry out apoptosis, we show that worms with an intermediate induction of apoptosis have the highest fertility level and most fit progeny during temperature stress. Second, we investigated an underlying genetic contribution to fertility and apoptosis levels during temperature stress by creating a novel recombinant inbred line panel using two strains with high or low fertility levels and apoptosis. We identified one quantitative trait locus associated with fertility level located on Chr II. Our results also show that worms with higher fertility also have higher apoptosis regardless of allele, and worms with the high fertility correlated allele have more apoptosis. Lastly, we show that temperature stress leads to more unpaired chromosomes in the oogenic nuclei, which results in apoptosis of the cell. We determined the canonical apoptosis pathway is triggered through parallel pathways: CED-13 inhibits CED-9 while LIN-35 and the DREAM complex down regulate ced-9 expression resulting in apoptosis of the oogenic nucleus. Collectively, this dissertation demonstrates that an increase in asynapsed chromosomes during moderate temperature stress leads to an induction of apoptosis that supplies additional cytoplasmic resources to cellularizing oocytes, buffering fertility and progeny fitness during moderate temperature stress. Our work provides a concrete example of germline stress-response strategy that will be imperative for the survival of species as elevated temperatures become more prevalent due to prolonged climate change.