Chromatin remodeler CHD7 targets active enhancer region to regulate cell type-specific gene expression in human neural crest cells

Tsukasa Sanosaka, Hironobu Okuno, Noriko Mizota, Tomoko Andoh-Noda, Miki Sato, Ryo Tomooka, Satoe Banno, Jun Kohyama, Hideyuki Okano

Research output: Contribution to journalArticlepeer-review

Abstract

A mutation in the chromatin remodeler chromodomain helicase DNA-binding 7 (CHD7) gene causes the multiple congenital anomaly CHARGE syndrome. The craniofacial anomalies observed in CHARGE syndrome are caused by dysfunctions of neural crest cells (NCCs), which originate from the neural tube. However, the mechanism by which CHD7 regulates the function of human NCCs (hNCCs) remains unclear. We aimed to characterize the cis-regulatory elements governed by CHD7 in hNCCs by analyzing genome-wide ChIP-Seq data and identifying hNCC-specific CHD7-binding profiles. We compared CHD7-binding regions among cell types, including human induced pluripotent stem cells and human neuroepithelial cells, to determine the comprehensive properties of CHD7-binding in hNCCs. Importantly, analysis of the hNCC-specific CHD7-bound region revealed transcription factor AP-2α as a potential co-factor facilitating the cell type-specific transcriptional program in hNCCs. CHD7 was strongly associated with active enhancer regions, permitting the expression of hNCC-specific genes to sustain the function of hNCCs. Our findings reveal the regulatory mechanisms of CHD7 in hNCCs, thus providing additional information regarding the transcriptional programs in hNCCs.

Original languageEnglish
Article number22648
JournalScientific reports
Volume12
Issue number1
DOIs
Publication statusPublished - 2022 Dec

ASJC Scopus subject areas

  • General

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