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The FMRFamide Neuropeptide FLP-20 Acts as a Systemic Signal for Starvation Responses in Caenorhabditis elegans

机译:FMRFamide神经肽FLP-20作为Caenorhabdise Labs中的饥饿反应的系统信号

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摘要

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.
机译:大多数动物在整个生命中面临繁殖的饥饿时期,因此需要在饥饿期间适当地调整它们的行为和代谢。这种适应性反应由一种复杂的全身信号调节,包括激素和神经肽。虽然在识别规范营养素过度状态的途径方面取得了很多进展,但仍然不完全理解动物如何系统地发信号缺乏状态。在这里,我们表明,FMRFamide神经肽FLP-20调节Caenorhabditis elegans的全身饥饿反应。我们发现FLP-20的突变通过抑制过量的自噬而拯救了G蛋白β-亚基GPB-2突变体的饥饿超敏反应。 FLP-20作用于AIB神经元,其中代谢谷氨酸受体MGL-2还用于调节全身饥饿反应。此外,FLP-20以依赖于受体型胍基环化酶GCY-28的方式调节饥饿诱导的脂肪降解。集体,我们的结果揭示了一种感官和信号营养缺乏状态来调节多细胞生物中的系统饥饿反应的电路。

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