Apoptosis during oogenesis is highly conserved in animals. During Caenorhabditis elegans oogenesis, roughly fifty percent of germ cells undergo apoptosis. While C. elegans oogenesis is widely studied, it is unclear why this mass cell death occurs. Under moderate temperature stress, there is a decrease in worm brood size but an increase germline apoptosis. There are two proposed hypotheses for the function of increased germline apoptosis that would aid in developing fit progeny under temperature stress. The first is that apoptotic cells serve as nurse cells, donating their cytoplasmic materials to developing oocytes. An increase in apoptosis during temperature stress may help ensure that developing oocytes receive sufficient cytoplasmic materials when an embryo is born under stress conditions. The second hypothesis is that apoptosis serves to remove defective cells that are made due to problems with oogenesis under moderate temperature stress. If the first hypothesis is correct and apoptotic cells act as nurse cells, an increase in apoptosis and thus an increase in cytoplasmic donations under temperature stress would also increase the rate of cytoplasmic streaming in the germline. Additionally, in mutants that have reduced apoptosis compared to wild type worms, the rate of cytoplasmic streaming would decrease compared to wild type animals at the same temperature. To test if increased apoptosis contributes increased amounts of cytoplasmic materials to developing oocytes, DIC microscopy was used to video tape live anesthetized young adult N2 worms raised at 20°C as well as worms upshifted to 26°C for 24 hours. Six worms were taped under both temperature conditions. Using ImageJ, five particles within the rachis of the germline were tracked in each worm over a two-minute period and each particles average velocity was calculated (n=30). Our analysis showed a significant increase in the rate of cytoplasmic streaming in worms upshifted to 26°C compared to worms raised at 20°C. Additional imaging is currently being performed on
lin-35 and
lin-54 mutants, which have been shown to have decreased apoptosis at high temperatures. Because these mutants do not show an increase in apoptosis under temperature stress, it is expected that their analysis will not show a significant increase in rate of cytoplasmic streaming as seen in the wildtype.