Homeostasis in C. elegans sleep is characterized by two behaviorally and genetically distinct mechanisms
Stanislav Nagy,
Nora Tramm,
Jarred Sanders,
Shachar Iwanir,
Ian A Shirley,
Erel Levine,
David Biron
Affiliations
Stanislav Nagy
Institute for Biophysical Dynamics, University of Chicago, Chicago, United States
Nora Tramm
Department of Physics, University of Chicago, Chicago, United States; James Franck Institute, University of Chicago, Chicago, United States
Jarred Sanders
Committee on Genetics, Genomics, and Systems Biology, University of Chicago, Chicago, United States
Shachar Iwanir
Department of Physics, University of Chicago, Chicago, United States; James Franck Institute, University of Chicago, Chicago, United States
Ian A Shirley
Department of Physics, University of Chicago, Chicago, United States; James Franck Institute, University of Chicago, Chicago, United States
Erel Levine
Department of Physics, Harvard University, Cambridge, United States; Center for Systems Biology, Harvard University, Cambridge, United States
David Biron
Institute for Biophysical Dynamics, University of Chicago, Chicago, United States; Department of Physics, University of Chicago, Chicago, United States; James Franck Institute, University of Chicago, Chicago, United States
Biological homeostasis invokes modulatory responses aimed at stabilizing internal conditions. Using tunable photo- and mechano-stimulation, we identified two distinct categories of homeostatic responses during the sleep-like state of Caenorhabditis elegans (lethargus). In the presence of weak or no stimuli, extended motion caused a subsequent extension of quiescence. The neuropeptide Y receptor homolog, NPR-1, and an inhibitory neuropeptide known to activate it, FLP-18, were required for this process. In the presence of strong stimuli, the correlations between motion and quiescence were disrupted for several minutes but homeostasis manifested as an overall elevation of the time spent in quiescence. This response to strong stimuli required the function of the DAF-16/FOXO transcription factor in neurons, but not that of NPR-1. Conversely, response to weak stimuli did not require the function of DAF-16/FOXO. These findings suggest that routine homeostatic stabilization of sleep may be distinct from homeostatic compensation following a strong disturbance.
