Mice lacking the chromodomain helicase DNA-binding 5 chromatin remodeler display autism-like characteristics.

ABSTRACT: Although autism spectrum disorders (ASDs) share a core set of nosological features, they exhibit substantial genetic heterogeneity. A parsimonious hypothesis posits that dysregulated epigenetic mechanisms represent common pathways in the etiology of ASDs. To investigate this hypothesis, we generated a novel mouse model resulting from brain-specific deletion of chromodomain helicase DNA-binding 5 (Chd5), a chromatin remodeling protein known to regulate neuronal differentiation and a member of a gene family strongly implicated in ASDs. RNA sequencing of Chd5^-/- mouse forebrain tissue revealed a preponderance of changes in expression of genes important in cellular development and signaling, sociocommunicative behavior and ASDs. Pyramidal neurons cultured from Chd5^-/- cor

SUBMITTER: Pisansky MT 

PROVIDER: S-EPMC5537637 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature