Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Jun 15;11:208. doi: 10.3389/fnmol.2018.00208

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2018 Lamar and Carvill.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Model for CHD2 role in chromatin remodeling and epilepsy. (A) During development, CHD2 is recruited to poised promoters with the bivalent histone modifications, H3K27me3 (repressive) and H3K4me3 (activating) by interaction with specific transcription factors. CHD2 remodels chromatin at target genes by replacing histone H3 with H3.3 and creating a more permissive chromatin state whereby transcription of developmental genes can occur during differentiation. (B) When CHD2 is mutated, promoters that would normally be poised for differentiation have an increase in the repressive H3K27me3 histone modification and H3.3 is not incorporated. These changes in the chromatin architecture restrict the expression of target genes during differentiation. During neuronal development this pathogenic mechanism likely leads to reduced expression of genes important in neuronal differentiation and impairments that ultimately lead to epilepsy and associated neurodevelopmental disorders.