RRC ID 45752
Author Hung WL, Wang Y, Chitturi J, Zhen M.
Title A Caenorhabditis elegans developmental decision requires insulin signaling-mediated neuron-intestine communication.
Journal Development
Abstract Adverse environmental conditions trigger C. elegans larvae to activate an alternative developmental program, termed dauer diapause, which renders them stress resistant. High-level insulin signaling prevents constitutive dauer formation. However, it is not fully understood how animals assess conditions to choose the optimal developmental program. Here, we show that insulin-like peptide (ILP)-mediated neuron-intestine communication plays a role in this developmental decision. Consistent with, and extending, previous findings, we show that the simultaneous removal of INS-4, INS-6 and DAF-28 leads to fully penetrant constitutive dauer formation, whereas the removal of INS-1 and INS-18 significantly inhibits constitutive dauer formation. These ligands are processed by the proprotein convertases PC1/KPC-1 and/or PC2/EGL-3. The agonistic and antagonistic ligands are expressed by, and function in, neurons to prevent or promote dauer formation. By contrast, the insulin receptor DAF-2 and its effector, the FOXO transcription factor DAF-16, function solely in the intestine to regulate the decision to enter diapause. These results suggest that the nervous system normally establishes an agonistic ILP-dominant paradigm to inhibit intestinal DAF-16 activation and allow reproductive development. Under adverse conditions, a switch in the agonistic-antagonistic ILP balance activates intestinal DAF-16, which commits animals to diapause.
Volume 141(8)
Pages 1767-79
Published 2014-4-1
DOI 10.1242/dev.103846
PII dev.103846
PMID 24671950
PMC PMC3978837
MeSH Animals Caenorhabditis elegans / growth & development* Caenorhabditis elegans / metabolism* Caenorhabditis elegans Proteins / metabolism Cell Communication* Green Fluorescent Proteins / metabolism Insulin / metabolism* Intestinal Mucosa / metabolism Intestines / cytology* Larva / metabolism Models, Biological Motor Neurons / cytology Motor Neurons / metabolism Neurons / cytology* Neurons / metabolism Sensory Receptor Cells / cytology Sensory Receptor Cells / metabolism Signal Transduction*
IF 5.611
Times Cited 43
C.elegans tm2308 tm1888 tm4467 tm3608 tm3620 tm2560 tm2416 tm2001 tm4144