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Fig. 7 | BMC Neuroscience

Fig. 7

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

Fig. 7

DAF-16 can act in multiple tissues to regulate sleep. Summary figure: decreased function of the Notch ligand lag-2 or loss of the stress response kinase jnk-1 increased total time in sleep bouts, dependent on DAF-16/FOXO function. Sleep is dependent on DAF-16 function in neurons of animals with decreased lag-2 function. The neurons and/or tissues where Notch DSL ligand LAG-2 functions in sleep regulation have not been identified. Previous work demonstrated that JNK-1 function is required in neurons for sleep bout quantity and sleep bout arousal thresholds. However, increased sleep in jnk-1 loss of function animals is dependent on DAF-16 function in muscles. We propose communication between muscles and neurons is required for DAF-16 dependent increased sleep in C. elegans L4/A lethargus and that DAF-16 can act in a non-cell-autonomous manner to regulate compensatory sleep bouts in jnk-1 mutant animals

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