論文 - 詳細
| RRC ID | 59562 |
|---|---|
| 著者 | Nagashima T, Iino Y, Tomioka M. |
| タイトル | DAF-16/FOXO promotes taste avoidance learning independently of axonal insulin-like signaling. |
| ジャーナル | PLoS Genet |
| Abstract |
The avoidance of starvation is critical for the survival of most organisms, thus animals change behavior based on past nutritional conditions. Insulin signaling is important for nutritional state-dependent behavioral plasticity, yet the underlying regulatory mechanism at the cellular level remains unclear. Previous studies showed that insulin-like signaling is required for taste avoidance learning, in which the nematode Caenorhabditis elegans avoids salt concentrations encountered under starvation conditions. DAF-2c, a splice isoform of the DAF-2 insulin receptor, functions in the axon of the ASER sensory neuron, which senses changes in salt concentrations. In addition, mutants of a major downstream factor of DAF-2, the forkhead transcription factor O (FOXO) homolog DAF-16, show defects in taste avoidance learning. Interestingly, the defect of the daf-2 mutant is not suppressed by daf-16 mutations in the learning, unlike those in other phenomena, such as longevity and development. Here we show that multiple DAF-16 isoforms function in ASER. By epistasis analysis using a DAF-2c isoform-specific mutant and an activated form of DAF-16, we found that DAF-16 acts in the nucleus in parallel with the DAF-2c-dependent pathway in the axon, indicating that insulin-like signaling acts both in the cell body and axon of a single neuron, ASER. Starvation conditioning induces nuclear translocation of DAF-16 in ASER and degradation of DAF-16 before starvation conditioning causes defects in taste avoidance learning. Forced nuclear localization of DAF-16 in ASER biased chemotaxis towards lower salt concentrtions and this effect required the Gq/PKC pathway and neuropeptide processing enzymes. These data imply that DAF-16/FOXO transmits starvation signals and modulates neuropeptide transmission in the learning. |
| 巻・号 | 15(7) |
| ページ | e1008297 |
| 公開日 | 2019-7-1 |
| DOI | 10.1371/journal.pgen.1008297 |
| PII | PGENETICS-D-19-00023 |
| PMID | 31323047 |
| PMC | PMC6668909 |
| MeSH | Animals Avoidance Learning / physiology* Behavior, Animal Caenorhabditis elegans / physiology* Caenorhabditis elegans Proteins / genetics* Caenorhabditis elegans Proteins / metabolism* Cell Nucleus / metabolism Epistasis, Genetic Forkhead Transcription Factors / genetics* Forkhead Transcription Factors / metabolism* Insulin Mutation Protein Isoforms / metabolism Receptor, Insulin / genetics Signal Transduction Sodium Chloride / analysis* |
| IF | 5.224 |
| 引用数 | 1 |
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オルトメトリクス指標項目
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| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 3 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| 線虫 | tm5030 tm5031 tm6659 tm718 |