Normal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep.

ABSTRACT:

Background

Sleep deprivation impairs learning, causes stress, and can lead to death. Notch and JNK-1 pathways impact C. elegans sleep in complex ways; these have been hypothesized to involve compensatory sleep. C. elegans DAF-16, a FoxO transcription factor, is required for homeostatic response to decreased sleep and DAF-16 loss decreases survival after sleep bout deprivation. Here, we investigate connections between these pathways and the requirement for sleep after mechanical stress.

Results

Reduced function of Notch ligand LAG-2 or JNK-1 kinase resulted in increased time in sleep bouts during development. These animals were inappropriately easy to arouse using sensory stimulation, but only during sleep bouts. This constellation of defects suggested that poor quality sleep

SUBMITTER: Bennett HL 

PROVIDER: S-EPMC5845181 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature