Neuronal regulation of systemic osmotic stress response mechanisms in C. elegans

Abstract

In C. elegans, 2 osmosensory ASH neurons function to detect hypertonic stress (HS) environments and activate a behavioral avoidance response. osm‐9 and osm‐12 encode proteins essential for ASH function. Worms lacking OSM‐9 or OSM‐12 activity exhibit defective HS avoidance. A central question in stress physiology is how animals exposed simultaneously to multiple acute and chronic stressors activate appropriate defense mechanisms that maximize survival as well as reproductive fitness. We tested the role of ASH neurons in HS resistance. osm‐9 and osm‐12 mutants showed greatly enhanced survival during HS compared to wild type (WT) worms. Improved HS survival is due to decreased water loss, more rapid volume recovery, constitutive glycerol accumulation and/or activation of proteostasis mechanisms to cope with HS‐induced protein damage. Mutant and WT worms exhibited similar water loss and volume recovery during HS. No constitutive activation of the glycerol accumulation pathway was detected in osm‐9 and osm‐12 mutants. These results suggest that signals from ASH neurons normally suppress the activity of proteostasis mechanisms in a cell non‐autonomous fashion. Neuronal control of proteostasis allows animals to regulate the allocation of cellular resources in manner that coordinates and maximizes their physiological requirements with their need to cope with acute and chronic environmental stressors.