Starvation-Signaling in the Nematode Caenorhabditis Elegans Using Regulator of G-Proteins GPB-2
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During starvation, C. elegans adjust their behavior in order to survive. Using the starvation-sensitive gpb-2(ad541) loss-of-function mutant, components in a starvation-signaling pathway were identified. The goals of the studies presented here were to identify neurons that propagate a starvation signal, and to identify genes that regulate fat storage in the gut during starvation. Starvation in gpb-2(ad541) worms is lethal, and this lethality can be induced by arecoline, an acetylcholine receptor antagonist. Starvation sensitivity in gpb-2(ad541) worms is inhibited by atropine, an acetylcholine receptor antagonist. Previous work suggests that cholinergic signaling propagates a starvation signal in the pharynx of the worm, and the MC neurons are responsible for sending that signal. By ablating the MC neurons in newly hatched L1 worms, I aimed to prevent starvation-induced lethality due to the gpb-2(ad541) background. Several genes have also been identified to act downstream of gpb-2 in the regulation of fat in the gut. Both flp-20 loss-of-function and mgl-2 loss-of-function mutations rescue the starvation-induced lethality of gpb-2(ad541), while introduction of a gcy-28 loss-of-function mutation restores lethality. When fat was assayed using Oil Red O, it was found that GCY-28, a receptor-type guanylate cyclase, is necessary to maintain fat levels during starvation. GCY-28 is expressed in various head neurons and throughout the gut, and GCY-28 may play a role in regulating how gut cells store fat.