The FMRFamide Neuropeptide FLP-20 Acts as a Systemic Signal for Starvation Responses in Caenorhabditis elegans.
The FMRFamide Neuropeptide FLP-20 Acts as a Systemic Signal for Starvation Responses in Caenorhabditis elegans.
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DOI：
10.14348/molcells.2021.0051
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发表时间：
2021-07-31
影响因子：
3.8
通讯作者：
Avery L
中科院分区：
文献类型：
--
作者：
Kang C;Avery L
大多数动物在其一生中经常面临饥饿，因此需要在饥饿期间适当调整其行为和代谢以维持生存。这种适应性反应是由一组复杂的系统信号调节的，包括激素和神经肽。虽然在确定调节营养过剩状态的途径方面取得了很大进展，但仍然不完全了解动物如何系统地发出营养缺乏状态的信号。在这里，我们表明，FMRFamide神经肽FLP-20调节秀丽隐杆线虫的系统饥饿反应。我们发现flp-20的突变通过抑制过度的自噬来挽救G蛋白β亚基gpb-2突变体的饥饿超敏性。FLP-20在AIB神经元中起作用，其中代谢型谷氨酸受体MGL-2也起调节全身饥饿反应的作用。此外，FLP-20调制饥饿诱导的脂肪降解的方式依赖于受体型鸟苷酸环化酶GCY-28。总的来说，我们的研究结果揭示了一个电路，传感和信号营养缺乏状态，以调节多细胞生物体的系统饥饿反应。
Most animals face frequent periods of starvation throughout their entire life and thus need to appropriately adjust their behavior and metabolism during starvation for their survival. Such adaptive responses are regulated by a complex set of systemic signals, including hormones and neuropeptides. While much progress has been made in identifying pathways that regulate nutrient-excessive states, it is still incompletely understood how animals systemically signal their nutrient-deficient states. Here, we showed that the FMRFamide neuropeptide FLP-20 modulates a systemic starvation response in Caenorhabditis elegans. We found that mutation of flp-20 rescued the starvation hypersensitivity of the G protein β-subunit gpb-2 mutants by suppressing excessive autophagy. FLP-20 acted in AIB neurons, where the metabotropic glutamate receptor MGL-2 also functions to modulate a systemic starvation response. Furthermore, FLP-20 modulated starvation-induced fat degradation in a manner dependent on the receptor-type guanylate cyclase GCY-28. Collectively, our results reveal a circuit that senses and signals nutrient-deficient states to modulate a systemic starvation response in multicellular organisms.