Pan-neuronal depletion of inc causes short sleep, while restoring inc solely to neurons is largely sufficient to rescue the sleep deficits of inc mutants, indicating that inc impacts sleep chiefly through neurons ( Pfeiffenberger and Allada, 2012 Stavropoulos and Young, 2011). Here, we assess the temporal contributions of insomniac ( inc), a gene whose mutation sharply curtails sleep in Drosophila ( Pfeiffenberger and Allada, 2012 Stavropoulos and Young, 2011). Notably, the temporal contributions of genes that impact sleep are rarely assessed in a comprehensive manner, and a further challenge has been linking particular genes to developmental processes that control the structure and function of discrete sleep-regulatory circuits. In contrast, despite great progress in understanding neuronal development ( Doe, 2008 Jessell and Sanes, 2000 Sanes and Zipursky, 2020 Tessier-Lavigne and Goodman, 1996 Weinstein and Hemmati-Brivanlou, 1999), developmental mechanisms by which genes influence sleep remain poorly explored, despite the likely relevance of such mechanisms to sleep disturbances in autism and other neurodevelopmental disorders ( Angriman et al., 2015 Souders et al., 2017). Chemelli et al., 1999 Lin et al., 1999), including with conditional gain-of-function, loss-of-function, and rescue in adult animals ( Chiu et al., 2016 Clasadonte et al., 2017 Foltenyi et al., 2007 Guo et al., 2011 Ishimoto and Kitamoto, 2010 Joiner et al., 2006 Van Buskirk and Sternberg, 2007). Genes that act in the adult brain to modulate the activity of sleep-regulatory circuits in an ongoing manner have been intensively investigated (e.g. While numerous genes that strongly impact sleep have been identified in humans and in animals ranging from mammals to invertebrates ( Chemelli et al., 1999 Chiu et al., 2016 Cirelli et al., 2005 Funato et al., 2016 He et al., 2009 Lin et al., 1999 Raizen et al., 2008), when these genes act to influence sleep is in many cases unresolved.
A central goal of sleep research has been elucidating the mechanisms by which genes shape normal sleep patterns and cause sleep disorders.
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