Neurohormonal signaling via a sulfotransferase antagonizes insulin-like signaling to regulate a Caenorhabditis elegans stress response

Nicholas O. Burton (), Vivek K. Dwivedi, Kirk B. Burkhart, Rebecca E. W. Kaplan, L. Ryan Baugh and H. Robert Horvitz ()
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Nicholas O. Burton: Massachusetts Institute of Technology
Vivek K. Dwivedi: Massachusetts Institute of Technology
Kirk B. Burkhart: Massachusetts Institute of Technology
Rebecca E. W. Kaplan: Duke University
L. Ryan Baugh: Duke University
H. Robert Horvitz: Massachusetts Institute of Technology

Nature Communications, 2018, vol. 9, issue 1, 1-9

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-07640-w

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