Neurohormonal signaling via a sulfotransferase antagonizes insulin-like signaling to regulate a Caenorhabditis elegans stress response
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Author(s)
Burton, Nicholas O
Dwivedi, Vivek Kumar
Burkhart, Kirk Benjamin
Kaplan, Rebecca D.
Baugh, Lauren
Horvitz, Howard Robert
Date Issued
December 2018
Journal
Nature Communications
Publisher
Nature Publishing Group
Citation
Burton, Nicholas O., Vivek K. Dwivedi, Kirk B. Burkhart, Rebecca E. W. Kaplan, L. Ryan Baugh, and H. Robert Horvitz. “Neurohormonal Signaling via a Sulfotransferase Antagonizes Insulin-Like Signaling to Regulate a Caenorhabditis Elegans Stress Response.” Nature Communications 9, no. 1 (December 2018).
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Final published version
Abstract
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.
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
Massachusetts Institute of Technology. Department of Biology
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
McGovern Institute for Brain Research at MIT
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Creative Commons Attribution 4.0 International license
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DOI of Published Version
https://doi.org/10.1038/s41467-018-07640-w
