Regulation of MAP Kinase signaling by the insulin-like growth factor pathway during C. elegans vulval development.

Abstract

Organ development depends on multiple signaling pathways working in concert to specify cell fates. Improper activity or inactivity of specific signaling pathways such as EGF-Ras-MAPK can lead to dedifferentiation and cancer. In C. elegans , gain of function mutations in Ras/ let-60 lead to ectopic development of multiple ventral vulva-like lesions resembling tumors. However, this phenotype depends on normal insulin-like growth factor (IGF) signaling. Here, we probe how factors downstream of the IGF receptor daf-2 modify Ras signaling. These investigations led us to identify regulators of cell fate such as the Zinc finger protein encoding gene mstr-1 ( F22D6.2 ), homologous to mammalian Zfand3 / 5 / 6 .