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Ins-4 and daf-28 function redundantly to regulate C. elegans L1 arrest.

Yutao Chen1, L Ryan Baugh1

  • 1Department of Biology, Duke Center for Systems Biology, Duke University, Durham, NC 27708, USA.

Developmental Biology
|August 17, 2014
PubMed
Summary

This study reveals how insulin-like peptides regulate Caenorhabditis elegans development during starvation-induced L1 arrest. Specific peptides like ins-4 and daf-28 are key to survival and development, showing functional overlap.

Keywords:
Caenorhabditis elegansDiapauseInsulinL1 arrestStarvation

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Area of Science:

  • Developmental Biology
  • Genetics
  • Molecular Biology

Background:

  • Caenorhabditis elegans larvae undergo reversible developmental arrest (L1 arrest) during starvation.
  • Insulin-like signaling is crucial for regulating this L1 arrest.
  • The roles of C. elegans' 40 insulin-like peptides in nutritional control of development are largely unknown.

Purpose of the Study:

  • To identify and characterize insulin-like peptides involved in the nutritional control of L1 development in C. elegans.
  • To understand the expression dynamics and spatial patterns of these peptides during L1 arrest and recovery.
  • To elucidate the functions of specific insulin-like genes in regulating L1 arrest and survival.

Main Methods:

  • High-resolution mRNA expression analysis of all 40 insulin-like genes during L1 arrest and recovery.
  • Identification of candidate insulin-like agonists and antagonists based on expression patterns.
  • Spatial expression analysis using destabilized reporter genes.
  • Phenotypic analysis of single and compound deletion mutants, and overexpression studies.

Main Results:

  • Nutrient availability significantly impacts the expression of most insulin-like genes, indicating complex regulation.
  • Thirteen candidate agonists and eight antagonists were identified; ten agonists were further studied.
  • Candidate agonists show overlapping expression in the intestine and key neurons (ASI, ASJ), with intestinal expression being most sensitive to nutrient status.
  • While single mutants showed no effect, ins-4 and daf-28 double mutants exhibited increased L1 arrest survival. Overexpression of ins-4, ins-6, or daf-28 reduced survival and promoted cell division during starvation.

Conclusions:

  • Insulin-like peptides exhibit extensive functional overlap in regulating L1 development and arrest in response to nutrition.
  • Insulin-4 (ins-4) and daf-28 play significant roles, with ins-6 having a lesser but notable contribution.
  • Intestinal nutrient status appears to be a primary driver for the transcriptional regulation of these developmental regulators.