insomniac links the development and function of a sleep-regulatory circuit

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 los...

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Published ineLife Vol. 10
Main Authors Li, Qiuling, Jang, Hyunsoo, Lim, Kayla Y, Lessing, Alexie, Stavropoulos, Nicholas
Format Journal Article
LanguageEnglish
Published England eLife Sciences Publications Ltd 15.12.2021
eLife Sciences Publications, Ltd
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Abstract 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. In mutants, MB neurons are produced in excess, develop anatomical defects that impede circuit assembly, and are unable to promote sleep when activated in adulthood. Our findings link neurogenesis and postmitotic development of sleep-regulatory neurons to their adult function and suggest that developmental perturbations of circuits that couple sensory inputs and sleep may underlie sleep dysfunction in neurodevelopmental disorders.
AbstractList Although many genes are known to influence sleep, when and how they impact sleep-regulatory circuits remain ill-defined. Here, we show that insomniac ( inc ), a conserved adaptor for the autism-associated Cul3 ubiquitin ligase, acts in a restricted period of neuronal development to impact sleep in adult Drosophila . The loss of inc causes structural and functional alterations within the mushroom body (MB), a center for sensory integration, associative learning, and sleep regulation. In inc mutants, MB neurons are produced in excess, develop anatomical defects that impede circuit assembly, and are unable to promote sleep when activated in adulthood. Our findings link neurogenesis and postmitotic development of sleep-regulatory neurons to their adult function and suggest that developmental perturbations of circuits that couple sensory inputs and sleep may underlie sleep dysfunction in neurodevelopmental disorders.
Although many genes are known to influence sleep, when and how they impact sleep-regulatory circuits remain ill-defined. Here, we show that insomniac (inc), a conserved adaptor for the autism-associated Cul3 ubiquitin ligase, acts in a restricted period of neuronal development to impact sleep in adult Drosophila. The loss of inc causes structural and functional alterations within the mushroom body (MB), a center for sensory integration, associative learning, and sleep regulation. In inc mutants, MB neurons are produced in excess, develop anatomical defects that impede circuit assembly, and are unable to promote sleep when activated in adulthood. Our findings link neurogenesis and postmitotic development of sleep-regulatory neurons to their adult function and suggest that developmental perturbations of circuits that couple sensory inputs and sleep may underlie sleep dysfunction in neurodevelopmental disorders.
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. In mutants, MB neurons are produced in excess, develop anatomical defects that impede circuit assembly, and are unable to promote sleep when activated in adulthood. Our findings link neurogenesis and postmitotic development of sleep-regulatory neurons to their adult function and suggest that developmental perturbations of circuits that couple sensory inputs and sleep may underlie sleep dysfunction in neurodevelopmental disorders.
Author Lim, Kayla Y
Stavropoulos, Nicholas
Li, Qiuling
Jang, Hyunsoo
Lessing, Alexie
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  organization: Waksman Institute, Rutgers University, Piscataway, United States
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Keywords neuroblast
sleep disorders
developmental biology
neuroscience
neurogenesis
Cul3
D. melanogaster
neurodevelopmental disorders
autism
Language English
License 2021, Li et al.
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Graduate Program in Molecular, Cellular, & Integrative Physiology, University of California, Los Angeles, United States.
Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea.
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Snippet 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...
Although many genes are known to influence sleep, when and how they impact sleep-regulatory circuits remain ill-defined. Here, we show that insomniac ( inc ),...
Although many genes are known to influence sleep, when and how they impact sleep-regulatory circuits remain ill-defined. Here, we show that insomniac (inc), a...
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Open Access Repository
Aggregation Database
Index Database
SubjectTerms Acids
Animals
Associative learning
Autism
Brain
Cul3
Developmental Biology
Drosophila melanogaster - genetics
Drosophila melanogaster - physiology
Drosophila Proteins - genetics
Drosophila Proteins - metabolism
Influence
Ligands
Mammals
Models, Animal
Mushroom bodies
Mushroom Bodies - physiology
Mutation
neuroblast
Neurodevelopmental disorders
Neurogenesis
Neuroscience
Sensory integration
Sleep
Sleep - genetics
Sleep disorders
Structure-function relationships
Ubiquitin
Ubiquitin-protein ligase
Variance analysis
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Title insomniac links the development and function of a sleep-regulatory circuit
URI https://www.ncbi.nlm.nih.gov/pubmed/34908527
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https://search.proquest.com/docview/2610412544
https://pubmed.ncbi.nlm.nih.gov/PMC8758140
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Volume 10
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