Indole induces acute paralysis followed by compensatory stress-induced sleep

Stress-induced sleep of <i>Caenorhabditis elegans</i> occurs following exposure to noxious stressors, such as pore forming toxins, extreme temperature, ultraviolet irradiation, tissue wounding, and viral infections. Enteropathogenic <i>Escherichia coli</i> (EPEC) is a pathogenic bacterium which can infect <i>C. elegans</i> , however stress-induced sleep in response to EPEC has not been investigated. EPEC affects worms via two distinct mechanisms: 1) Contact-independent paralysis which occurs following the release of the toxin indole; 2) Contact-dependent bacterial colonization of the intestine. Here we examine mechanism one; we find that indole induced paralysis is regulated independently of the ALA and RIS sleep neurons. In fact, impairing ALA and RIS function caused animals to paralyze significantly faster than controls. Increasing cholinergic or GABAergic input, accelerated or delayed paralysis, respectively. Worms exposed to indole who were subsequently rescued to normal growth plates displayed a compensatory stress-induced sleep that was RIS but not ALA dependent. This work will allow for detailed future investigations into indole's mechanism of action, EPEC pathogenicity, and how bacterial infection leads to recovery sleep.