Mutations in Cullin-3 (Cul3), a conserved gene encoding a ubiquitin ligase, are strongly associated with autism spectrum disorder (ASD). Here, we characterize ASD-related pathologies caused by neuron-specific Cul3 knockdown in Drosophila. We confirmed that neuronal Cul3 knockdown causes short sleep, paralleling sleep disturbances in ASD.
View Article and Find Full Text PDFBackground: The number of total knee arthroplasty (TKA) procedures performed annually is increasing for reasons not fully explained by population growth and increasing rates of obesity. The purpose of this study was to determine the role of patient functional status as an indication for surgery and to determine if patients are undergoing surgery with a higher level of preoperative function than in the past.
Methods: A systematic review and meta-analysis of the MEDLINE, Embase and Cochrane databases was performed in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines.
Although many genes are known to influence sleep, when and how they impact sleep-regulatory circuits remain ill-defined. Here, we show that (), a conserved adaptor for the autism-associated Cul3 ubiquitin ligase, acts in a restricted period of neuronal development to impact sleep in adult . The loss of causes structural and functional alterations within the mushroom body (MB), a center for sensory integration, associative learning, and sleep regulation.
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