Disruption of grin2B, an ASD-associated gene, produces social deficits in zebrafish.

ABSTRACT:

Background

Autism spectrum disorder (ASD), like many neurodevelopmental disorders, has complex and varied etiologies. Advances in genome sequencing have identified multiple candidate genes associated with ASD, including dozens of missense and nonsense mutations in the NMDAR subunit GluN2B, encoded by GRIN2B. NMDARs are glutamate-gated ion channels with key synaptic functions in excitatory neurotransmission. How alterations in these proteins impact neurodevelopment is poorly understood, in part because knockouts of GluN2B in rodents are lethal.

Methods

Here, we use CRISPR-Cas9 to generate zebrafish lacking GluN2B (grin2B^-/-). Using these fish, we run an array of behavioral tests and perform whole-brain larval imaging to assay developmental roles and functions of Gl

SUBMITTER: Zoodsma JD 

PROVIDER: S-EPMC9502958 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature