Systemic regulation of starvation response in Caenorhabditis elegans

Systemic regulation of starvation response in Caenorhabditis elegans
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DOI:
10.1101/gad.1723409
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发表时间:
2009-01-01
影响因子:
10.5
通讯作者:
Avery, Leon
Avery, Leon
中科院分区:
生物学1区
文献类型:
--
作者:
Kang, Chanhee;Avery, Leon

文献摘要

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当环境营养物质供应有限时,多细胞动物可以通过生理和行为的变化来科普营养饥饿。虽然饥饿的生理和行为影响是众所周知的,但动物系统感知饥饿的机制仍然难以捉摸。此外,食物的哪些成分被感知以及它如何调节饥饿反应仍然知之甚少。在这项研究中,我们使用一个饥饿过敏突变体,以确定调节饥饿信号的分子和机制。我们发现,特定的氨基酸可以抑制饥饿诱导的死亡gpb-2突变体,和MGL-1和MGL-2,秀丽隐杆线虫同源的代谢型谷氨酸受体,参与。MGL-1和MGL-2分别作用于AIY和AIB神经元。亮氨酸处理抑制了野生型蠕虫饥饿诱导的应激抵抗力和寿命延长,而mgl-1和mgl-2的突变消除了亮氨酸的这些作用。综上所述,我们的结果表明,AIY和AIB神经元中的代谢型谷氨酸受体同源物可能调节系统性饥饿反应,而C。线虫能感知特定的氨基酸作为抗饥饿信号。
When the supply of environmental nutrients is limited, multicellular animals can make both physiological and behavioral changes so as to cope with nutrient starvation. Although physiological and behavioral effects of starvation are well known, the mechanisms by which animals sense starvation systemically remain elusive. Furthermore, what constituent of food is sensed and how it modulates starvation response is still poorly understood. In this study, we use a starvation-hypersensitive mutant to identify molecules and mechanisms that modulate starvation signaling. We found that specific amino acids could suppress the starvation-induced death of gpb-2 mutants, and that MGL-1 and MGL-2, Caenorhabditis elegans homologs of metabotropic glutamate receptors, were involved. MGL-1 and MGL-2 acted in AIY and AIB neurons, respectively. Treatment with leucine suppressed starvation-induced stress resistance and life span extension in wild-type worms, and mutation of mgl-1 and mgl-2 abolished these effects of leucine. Taken together, our results suggest that metabotropic glutamate receptor homologs in AIY and AIB neuron may modulate a systemic starvation response, and that C. elegans senses specific amino acids as an anti-hunger signal.