CRISPR/Cas9-induced shank3b mutant zebrafish display autism-like behaviors.

ABSTRACT:

Background

Human genetic and genomic studies have supported a strong causal role of SHANK3 deficiency in autism spectrum disorder (ASD). However, the molecular mechanism underlying SHANK3 deficiency resulting in ASD is not fully understood. Recently, the zebrafish has become an attractive organism to model ASD because of its high efficiency of genetic manipulation and robust behavioral phenotypes. The orthologous gene to human SHANK3 is duplicated in the zebrafish genome and has two homologs, shank3a and shank3b. Previous studies have reported shank3 morphants in zebrafish using the morpholino method. Here, we report the generation and characterization of shank3b mutant zebrafish in larval and adult stages using the CRISPR/Cas9 genom

SUBMITTER: Liu CX 

PROVIDER: S-EPMC5879542 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature