P53- and ERK7-dependent ribosome surveillance response regulates Drosophila insulin-like peptide secretion.

ABSTRACT: Insulin-like signalling is a conserved mechanism that coordinates animal growth and metabolism with nutrient status. In Drosophila, insulin-producing median neurosecretory cells (IPCs) regulate larval growth by secreting insulin-like peptides (dILPs) in a diet-dependent manner. Previous studies have shown that nutrition affects dILP secretion through humoral signals derived from the fat body. Here we uncover a novel mechanism that operates cell autonomously in the IPCs to regulate dILP secretion. We observed that impairment of ribosome biogenesis specifically in the IPCs strongly inhibits dILP secretion, which consequently leads to reduced body size and a delay in larval development. This response is dependent on p53, a known surveillance factor for ribosome biogenesis. A downstream effect

SUBMITTER: Hasygar K 

PROVIDER: S-EPMC4230838 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature