PT  - JOURNAL ARTICLE
AU  - Rosalind Hussey
AU  - Emily Witham
AU  - Erik Vanstrum
AU  - Jaleh Mesgarzadeh
AU  - Harkaranveer Ratanpal
AU  - Supriya Srinivasan
TI  - Oxygen-sensing neurons reciprocally regulate peripheral lipid metabolism via neuropeptide signaling in <em>Caenorhabditis elegans</em>
AID  - 10.1101/142422
DP  - 2017 Jan 01
TA  - bioRxiv
PG  - 142422
4099  - http://biorxiv.org/content/early/2017/05/25/142422.short
4100  - http://biorxiv.org/content/early/2017/05/25/142422.full
AB  - The mechanisms by which the sensory environment instructs 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.