RRC ID 3552
Author Tomioka M, Adachi T, Suzuki H, Kunitomo H, Schafer WR, Iino Y.
Title The insulin/PI 3-kinase pathway regulates salt chemotaxis learning in Caenorhabditis elegans.
Journal Neuron
Abstract The insulin-like signaling pathway is known to regulate fat metabolism, dauer formation, and longevity in Caenorhabditis elegans. Here, we report that this pathway is also involved in salt chemotaxis learning, in which animals previously exposed to a chemoattractive salt under starvation conditions start to show salt avoidance behavior. Mutants of ins-1, daf-2, age-1, pdk-1, and akt-1, which encode the homologs of insulin, insulin/IGF-I receptor, PI 3-kinase, phosphoinositide-dependent kinase, and Akt/PKB, respectively, show severe defects in salt chemotaxis learning. daf-2 and age-1 act in the ASER salt-sensing neuron, and the activity level of the DAF-2/AGE-1 pathway in this neuron determines the extent and orientation of salt chemotaxis. On the other hand, ins-1 acts in AIA interneurons, which receive direct synaptic inputs from sensory neurons and also send synaptic outputs to ASER. These results suggest that INS-1 secreted from AIA interneurons provides feedback to ASER to generate plasticity of chemotaxis.
Volume 51(5)
Pages 613-25
Published 2006-9-7
DOI 10.1016/j.neuron.2006.07.024
PII S0896-6273(06)00589-7
PMID 16950159
MeSH 3-Phosphoinositide-Dependent Protein Kinases Animals Caenorhabditis elegans / physiology* Caenorhabditis elegans Proteins / genetics Caenorhabditis elegans Proteins / metabolism Chemotaxis / physiology* Immunohistochemistry Insulin / metabolism* Interneurons / metabolism Learning / physiology* Mutation Neurons, Afferent / metabolism Phosphatidylinositol 3-Kinases / metabolism* Protein Serine-Threonine Kinases / genetics Protein Serine-Threonine Kinases / metabolism Proto-Oncogene Proteins c-akt / genetics Proto-Oncogene Proteins c-akt / metabolism Receptor, Insulin / genetics Receptor, Insulin / metabolism Signal Transduction / physiology* Sodium Chloride / metabolism
IF 14.415
Times Cited 168
WOS Category NEUROSCIENCES
Resource
C.elegans tm501