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

## TL;DR

The paper explores how insulin-like growth factor signaling influences MAP kinase activity during vulval development in C. elegans.

## Contribution

The study identifies a novel regulator of cell fate, mstr-1, linked to mammalian Zfand3/5/6, in the context of Ras and IGF signaling.

## Key findings

- Gain-of-function mutations in let-60 cause tumor-like lesions dependent on IGF signaling.
- The gene mstr-1 is identified as a downstream regulator of IGF signaling affecting Ras activity.
- mstr-1 is homologous to mammalian Zfand3/5/6, suggesting evolutionary conservation.

## 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
.