Neurohormonal signaling via a sulfotransferase antagonizes insulin-like signaling to regulate a Caenorhabditis elegans stress response.,Nature Communications

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Neurohormonal signaling via a sulfotransferase antagonizes insulin-like signaling to regulate a Caenorhabditis elegans stress response.
Nature Communications ( IF 14.7 ) Pub Date : 2018-12-04 , DOI: 10.1038/s41467-018-07640-w
Nicholas O Burton _{1,

2} , Vivek K Dwivedi ₁ , Kirk B Burkhart ₁ , Rebecca E W Kaplan ₃ , L Ryan Baugh ₃ , H Robert Horvitz ₁

Affiliation

Insulin and insulin-like signaling regulates a broad spectrum of growth and metabolic responses to a variety of internal and environmental stimuli. For example, the inhibition of insulin-like signaling in C. elegans mediates its response to both osmotic stress and starvation. We report that in response to osmotic stress the cytosolic sulfotransferase SSU-1 antagonizes insulin-like signaling and promotes developmental arrest. Both SSU-1 and the DAF-16 FOXO transcription factor, which is activated when insulin signaling is low, are needed to drive specific responses to reduced insulin-like signaling. We demonstrate that SSU-1 functions in a single pair of sensory neurons to control intercellular signaling via the nuclear hormone receptor NHR-1 and promote both the specific transcriptional response to osmotic stress and altered lysophosphatidylcholine metabolism. Our results show the requirement of a sulfotransferase-nuclear hormone receptor neurohormonal signaling pathway for some but not all consequences of reduced insulin-like signaling.

中文翻译：

通过磺基转移酶的神经激素信号传导拮抗胰岛素样信号传导，以调节秀丽隐杆线虫应激反应。

胰岛素和类胰岛素信号传导调节对各种内部和环境刺激的广泛生长和代谢反应。例如，线虫中胰岛素样信号传导的抑制介导其对渗透压和饥饿的反应。我们报告说，为了应对渗透压，胞质磺基转移酶 SSU-1 会拮抗胰岛素样信号传导并促进发育停滞。 SSU-1 和 DAF-16 FOXO 转录因子在胰岛素信号传导较低时被激活，需要驱动对胰岛素样信号传导减少的特定反应。我们证明 SSU-1 在一对感觉神经元中发挥作用，通过核激素受体 NHR-1 控制细胞间信号传导，并促进对渗透压的特异性转录反应和改变的溶血磷脂酰胆碱代谢。我们的结果表明，磺基转移酶-核激素受体神经激素信号传导途径需要磺基转移酶-核激素受体神经激素信号传导途径来实现胰岛素样信号传导减少的一些但不是全部后果。

更新日期：2018-12-04

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