Figure 9 .

Model for the ime-2 and vib-1 genetic pathway. (A) VIB-1 positively regulates HI and cell death, as well as HET domain gene expression (via a separate mechanism). IME-2 negatively regulates additional HI cell death mediators that function in parallel to the VIB-1 pathway. Due to the role of IME-2 in the processing of a mitochondrial protein, we reasoned that the alternate cell-death effectors and/or pathway could be acting through the mitochondria. Further, since deletions in ime-2 do not exhibit increased cell death during HI, we suggest that VIB-1 negatively regulates these alternate death effectors. (B) VIB-1 also positively regulates secreted proteases and, similar to the mechanism for HI cell-death regulation, IME-2 negatively regulates a parallel pathway for secreted proteases. Deletions in ime-2 cause a significant increase in secreted proteases, and thus in this pathway, VIB-1 does not regulate the parallel pathway for secreted proteases. Further, IME-2 appears to negatively regulate VIB-1 with respect to protoperithecial development via a separate pathway. For both pathways, it is likely that IME-2 is regulated by cellular signals of nitrogen availability.