The Insulin/Pi 3-kinase Pathway Regulates Salt Chemotaxis Learning in Caenorhabditis Elegans.
From: Molecular Genetics Research Laboratory, Graduate School of Science, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.
Neuron
- Publish Date: Sep 2006
- ISSN: 0896-6273
- Volume: 51
- Issue: 5
- Pages: 613-25
- Medium: Print
- Language: English
- Citation (JAMA): Tomioka Masahiro, Adachi Takeshi, Suzuki Hiroshi, et al. The Insulin/Pi 3-kinase Pathway Regulates Salt Chemotaxis Learning in Caenorhabditis Elegans.. Neuron Sep 2006;51:613-25
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.
Mesh Headings (Keywords): 1-Phosphatidylinositol 3-Kinase, Animals, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Chemotaxis, Immunohistochemistry, Insulin, Interneurons, Learning, Mutation, Neurons, Afferent, Protein-Serine-Threonine Kinases, Proto-Oncogene Proteins c-akt, Receptor, Insulin, Signal Transduction, Sodium Chloride
Check for Full Text / PubMed Unique Identifier (PMID): 16950159
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