Selected Publications
Homeostasis in *C. elegans* sleep is characterized by two behaviorally and genetically distinct mechanisms
Disrupting nematode sleep revealed two distinct homeostatic behaviors depending on whether the stimulus was strong or weak. I found distinct molecular pathways and cells that regulate these behaviors. Following weak stimuli, neuropeptide signaling through NPR-1 was needed for a brief extension of quiescence. I later found that NPR-1 is needed only in the RMG neurons for this behavior to occur (data not shown in paper). In contrast, a sustained elevation in quiescence following strong stimuli required the stress-activated transcription factor DAF-16/FoxO. Expression of DAF-16 in neurons but not in the muscles or intestine was required for this homeostatic response. Moreover, DAF-16 was not needed for the homeostatic response to weak stimuli, and NPR-1 was unnecessary for the response to strong stimuli.
In eLife