期刊
AUTOPHAGY
卷 5, 期 4, 页码 565-566出版社
LANDES BIOSCIENCE
DOI: 10.4161/auto.5.4.8171
关键词
autophagy; starvation; metabotropic glutamate receptor; amino acid response; Caenorhabditis elegans; hormesis
类别
资金
- NHLBI NIH HHS [R01 HL046154, R01 HL046154-13, HL 46154, R37 HL046154] Funding Source: Medline
When no supply of environmental nutrients is available, cells induce autophagy, thereby generating a source of emergency metabolic substrates and energy to maintain the basal cellular activity needed for survival. This autophagy response to starvation has been well characterized in various multicellular organisms, including worms, flies and mice. Although prosurvival effects of autophagy in response to starvation are well known in animals, the mechanisms by which animals regulate and coordinate autophagy systemically remain elusive. Using C elegans as a model system, we found that specific amino acids could regulate starvation-induced autophagy, and that MGL-1 and MGL-2, Caenorhabditis elegans homologs of metabotropic glutamate receptors, were involved. MGL-1 and MGL-2 specifically acted in AIY and AIB neurons, respectively, to modulate the autophagy response in other tissues such as pharyngeal muscle. Our recent study suggests that the autophagy response to starvation, previously thought to be cell-autonomous, can be systemically regulated, and that there is a specific sensor for monitoring systemic amino acids levels in Caenorhabditis elegans.
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