biostudies-literatureBennett HLBrown Institute for Brain Science and Norman Prince Neurosciences Institute Postdoctoral Fellowship in Translational NeuroscienceUniversity of Pennsylvania Postdoctoral Opportunities in Research and TeachingInitiative to Maximize Student Development Training GrantNINDS NIH HHSNational Institutes of HealthNIH Office of Research Infrastructure ProgramsNIGMS NIH HHSKaren T. Romer Undergraduate Teaching and Research AwardNIH HHSNational Science Foundation10https://www.ebi.ac.uk/biostudies/studies/S-EPMC5845181biostudies-literatureUnknown19(1)<h4>Background</h4>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.<h4>Results</h4>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 sleepBMC neuroscienceNormal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep.PMC5845181NS055813(P40 OD010440)R25GM083270NIH R01 GM078171K12 GM081259K12 GM081259-10P40 OD010440IOS 1256989R25 GM083270R01 NS055813R01 GM078171Sanders JKhoruzhik YHart ACHuang HWalsh MBBiron DBennett HLHayden DfalseNormal sleep bouts are not essential for C. elegans survival and FoxO is important for compensatory changes in sleep.<h4>Background</h4>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.<h4>Results</h4>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 sleep2018-01-01T00:00:00Z2018 Mar2025-04-19T07:24:23.104Z2019-03-26T23:17:59ZS-EPMC58451812952307610.1186/s12868-018-0408-1