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Autism-linked Cullin3 germline haploinsufficiency impacts cytoskeletal dynamics and cortical neurogenesis through RhoA signaling

by Zhang, Pan , Qiu, Lily R , Urresti Jorge , Sebat, Jonathan , Lerch, Jason P , Herrera, Victor Munive , Pramod Akula Bala , Amar Megha , Trujillo, Cleber A , Diedrich Jolene , Chen, Jiaye , Yates, John R , Nam-Kyung, Yu , Iakoucheva Lilia M , Chau, Kevin , Ramanathan Dhakshin , Gutierrez, Jessica , Ellegood Jacob , Muotri Alysson R , Moran-Losada, Patricia

in Actin / Autism / Cognitive ability / CRISPR / Cytoskeleton / Embryogenesis / Genome editing / Genomes / Haploinsufficiency / Magnetic resonance imaging / Mutants / Mutation / Neurogenesis / Phenotypes / Proteomics / RhoA protein / Ubiquitin / Ubiquitin-protein ligase

2021

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Autism-linked Cullin3 germline haploinsufficiency impacts cytoskeletal dynamics and cortical neurogenesis through RhoA signaling

2021

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Autism-linked Cullin3 germline haploinsufficiency impacts cytoskeletal dynamics and cortical neurogenesis through RhoA signaling

2021

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Journal Article

Autism-linked Cullin3 germline haploinsufficiency impacts cytoskeletal dynamics and cortical neurogenesis through RhoA signaling

Zhang, Pan,

Qiu, Lily R,

Urresti Jorge,

Sebat, Jonathan,

Lerch, Jason P,

Herrera, Victor Munive,

Pramod Akula Bala,

Amar Megha,

Trujillo, Cleber A,

Diedrich Jolene,

Chen, Jiaye,

Yates, John R,

Nam-Kyung, Yu,

Iakoucheva Lilia M,

Chau, Kevin,

Ramanathan Dhakshin,

Gutierrez, Jessica,

Ellegood Jacob,

Muotri Alysson R,

Moran-Losada, Patricia

2021

Overview

E3-ubiquitin ligase Cullin3 (Cul3) is a high confidence risk gene for autism spectrum disorder (ASD) and developmental delay (DD). To investigate how Cul3 mutations impact brain development, we generated a haploinsufficient Cul3 mouse model using CRISPR/Cas9 genome engineering. Cul3 mutant mice exhibited social and cognitive deficits and hyperactive behavior. Brain MRI found decreased volume of cortical regions and changes in many other brain regions of Cul3 mutant mice starting from early postnatal development. Spatiotemporal transcriptomic and proteomic profiling of embryonic, early postnatal and adult brain implicated neurogenesis and cytoskeletal defects as key drivers of Cul3 functional impact. Specifically, dendritic growth, filamentous actin puncta, and spontaneous network activity were reduced in Cul3 mutant mice. Inhibition of small GTPase RhoA, a molecular substrate of Cul3 ligase, rescued dendrite length and network activity phenotypes. Our study identified defects in neuronal cytoskeleton and Rho signaling as the primary targets of Cul3 mutation during brain development.

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Publisher

Nature Publishing Group

Subject

/ Autism

/ CRISPR