Systemic regulation of autophagy in Caenorhabditis elegans.
Systemic regulation of autophagy in Caenorhabditis elegans.
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DOI：
10.4161/auto.5.4.8171
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发表时间：
2009-05
期刊：
影响因子：
13.3
通讯作者：
Avery L
中科院分区：
文献类型：
--
作者：
Kang C;Avery L
当没有环境营养物质供应时，细胞诱导自噬，从而产生紧急代谢底物和能量的来源，以维持生存所需的基本细胞活性。这种对饥饿的自噬反应已经在各种多细胞生物中得到了很好的表征，包括蠕虫，苍蝇和小鼠。虽然自噬对饥饿反应的促生存作用在动物中是众所周知的，但动物系统地调节和协调自噬的机制仍然难以捉摸。利用C.以线虫为模型系统，我们发现特定的氨基酸可以调控饥饿诱导的自噬，并且线虫代谢型谷氨酸受体的同源物MGL-1和MGL-2参与了调控。MGL-1和MGL-2分别特异性作用于AIY和AIB神经元，以调节其他组织如咽肌中的自噬反应。我们最近的研究表明，对饥饿的自噬反应，以前被认为是细胞自主的，可以系统调节，并且有一个特定的传感器用于监测秀丽隐杆线虫的系统氨基酸水平。
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.