Oxygen-sensing neurons reciprocally regulate peripheral lipid metabolism via neuropeptide signaling in Caenorhabditis elegans

Rosalind Hussey, Nicole K. Littlejohn, Emily Witham, Erik Vanstrum, Jaleh Mesgarzadeh, Harkaranveer Ratanpal, Supriya Srinivasan

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

The mechanisms by which the sensory environment influences metabolic homeostasis remains poorly understood. In this report, we show that oxygen, a potent environmental signal, is an important regulator of whole body lipid metabolism. C. elegans oxygen-sensing neurons reciprocally regulate peripheral lipid metabolism under normoxia in the following way: under high oxygen and food absence, URX sensory neurons are activated, and stimulate fat loss in the intestine, the major metabolic organ for C. elegans. Under lower oxygen conditions or when food is present, the BAG sensory neurons respond by repressing the resting properties of the URX neurons. A genetic screen to identify modulators of this effect led to the identification of a BAG-neuron-specific neuropeptide called FLP-17, whose cognate receptor EGL-6 functions in URX neurons. Thus, BAG sensory neurons counterbalance the metabolic effect of tonically active URX neurons via neuropeptide communication. The combined regulatory actions of these neurons serve to precisely tune the rate and extent of fat loss to the availability of food and oxygen, and provides an interesting example of the myriad mechanisms underlying homeostatic control.

Original languageEnglish
Article numbere1007305
JournalPLoS Genetics
Issue number3
Publication statusPublished - 26 Mar 2018

Keywords / Materials (for Non-textual outputs)

  • Animals
  • Caenorhabditis elegans/metabolism
  • Cell Communication
  • Guanylate Cyclase/metabolism
  • Intestinal Mucosa/metabolism
  • Lipid Metabolism
  • Neuropeptides/metabolism
  • Oxygen/metabolism
  • Sensory Receptor Cells/metabolism
  • Signal Transduction


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