|Keywords:||PTEN; C. elegans; starvation; L1 arrest; insulin signalling; DAF-18|
|Full text PDF:||http://qspace.library.queensu.ca/bitstream/1974/12697/3/Chamberlain_Gabriel_S_201512_MSc.pdf|
The insulin signaling antagonist daf-18/PTEN is known to play various roles in the response of C. elegans to starvation. While daf-18’s roles in promoting dauer formation are well understood, the extent of its roles in L1 arrest remains unclear. Recent studies have highlighted the importance of germline expression of daf-18 in coordinating proper L1 arrest. It had been previously hypothesized that germline expressed daf-18 might be sufficient to properly arrest germline proliferation and achieve wildtype levels of L1 arrest longevity. In this study, I show that germline expression alone is neither sufficient in restoring full L1 arrest longevity nor germ cell quiescence. Instead, L1 arrest longevity is dependent on systemic daf-18 expression. I also explore the effects of maternal contributions to offspring on L1 arrest longevity. I show here that maternally rescued daf-18 mutants survive two days longer than controls. I demonstrate that worms that progressed to adulthood through the dauer life stage do not produce offspring that are better suited to survive L1 arrest. Conversely, I observed adult worms that experience crowding produce offspring with mildly increased L1 arrest longevity. Lastly, I explore the post- translational regulation of DAF-18 by demonstrating that the proteasomal subunits pas-3 and pbs-4 are involved in DAF-18 degradation.