Sleep disturbances in autism and neurodevelopmental disorders are common and adversely affect patient’s quality of life, yet the underlying mechanisms are understudied. We found that individuals with mutations in CHD8, among the highest-confidence autism risk genes, or CHD7 suffer from disturbed sleep maintenance. These defects are recapitulated in Drosophila mutants affecting kismet, the sole CHD8/CHD7 ortholog. We show that Kismet is required in glia for early developmental and adult sleep architecture. This role localizes to subperineurial glia constituting the blood-brain barrier. We demonstrate that Kismet-related sleep disturbances are caused by high serotonin during development, paralleling a well-established but genetically unsolved autism endophenotype. Despite their developmental origin, Kismet’s sleep architecture defects can be reversed in adulthood by a behavioral regime resembling human sleep restriction therapy. Our findings provide fundamental insights into glial regulation of sleep and propose a causal mechanistic link between the CHD8/CHD7/Kismet family, developmental hyperserotonemia, and autism-associated sleep disturbances.

Direct Link:

Journal: Science Advances. 2021 Jun 1;7(23):eabe2626.

Keywords: ASD, autism, kismet, serotonin, Sleep,

Applications: Sleep,

CamNtech Reference: M21039

Back to Search Results

UK & International customers

CamNtech Ltd.
Manor Farm
PE28 9JD, UK

US customers

CamNtech Inc.
630 Boerne Stage Airfield,
Texas 78006,


© 2022 CamNtech Ltd and CamNtech Inc

Company information

Registered in England No. 2221302
VAT No: GB486 3019 34

Privacy Policy