Nathan Rather / Biology / Faculty Mentor: Piya Ghose
Programmed cell death (PCD) plays a critical role in conferring organismal development and homeostasis. We discovered a non-canonical apoptotic developmental cell death program in the C. elegans tail spike cell (TSC) called Compartmentalized Cell Elimination (CCE). During CCE three distinct parts of the cell die differently. A forward genetic screen for CCE defects recovered a mutant, ns957, that shows a persisting enlarged soma. Genetic analysis of ns957 revealed that the causative lesion is a mutation in eor-1. Here we report a novel role for the EOR-1/2 as well as its cofactors in CCE. Interestingly, EOR-1 has been implicated in other forms of cell death although its mechanism remains unknown. We find that caspase protease activity is normal in eor-1(-), suggesting that EOR-1 acts downstream of caspase in CCE. The soma remnant of an eor-1(-); ced-12(-) double mutant does not appear as a refractile cell nor as a living cell, suggesting that it is a quasi-living cell. Using a candidate gene approach based on putative EOR-1 transcriptional targets we found that mutants for wah-1, which encodes a mitochondrial oxidoreductase, phenocopy eor-1(-) soma phenotype. Here, we suggest that the EOR-1 transcription factor and WAH-1 act to promote soma elimination during CCE.
Leave a Reply