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Elife. 2014 Dec 4;3:e04380. doi: 10.7554/eLife.04380.

Homeostasis in C. elegans sleep is characterized by two behaviorally and genetically distinct mechanisms.

Author information

1
Institute for Biophysical Dynamics, University of Chicago, Chicago, United States.
2
Department of Physics, University of Chicago, Chicago, United States.
3
Committee on Genetics, Genomics, and Systems Biology, University of Chicago, Chicago, United States.
4
Department of Physics, Harvard University, Cambridge, United States.

Abstract

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.

KEYWORDS:

C. elegans; homeostasis; insulin; lethargus; neuropeptides; neuroscience; quiescence; sleep

PMID:
25474127
PMCID:
PMC4273442
DOI:
10.7554/eLife.04380
[Indexed for MEDLINE]
Free PMC Article

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