The Mechanism of Chromatin Remodeler SMARCAD1/Fun30 in Response to DNA Damage

Ze-Bin Tong; Hua-Song Ai; Jia-Bin Li

doi:10.3389/fcell.2020.560098

The Mechanism of Chromatin Remodeler SMARCAD1/Fun30 in Response to DNA Damage

Front Cell Dev Biol. 2020 Sep 25:8:560098. doi: 10.3389/fcell.2020.560098. eCollection 2020.

Authors

Ze-Bin Tong^{1

2}, Hua-Song Ai², Jia-Bin Li¹

Affiliations

¹ College of Pharmaceutical Sciences, Soochow University, Suzhou, China.
² Ministry of Education Key Laboratory of Bioorganic Phosphorus Chemistry and Chemical Biology, Department of Chemistry, Tsinghua University, Beijing, China.

Abstract

DNA packs into highly condensed chromatin to organize the genome in eukaryotes but occludes many regulatory DNA elements. Access to DNA within nucleosomes is therefore required for a variety of biological processes in cells including transcription, replication, and DNA repair. To cope with this problem, cells employ a set of specialized ATP-dependent chromatin-remodeling protein complexes to enable dynamic access to packaged DNA. In the present review, we summarize the recent advances in the functional and mechanistic studies on a particular chromatin remodeler SMARCAD1^Fun30 which has been demonstrated to play a key role in distinct cellular processes and gained much attention in recent years. Focus is given to how SMARCAD1^Fun30 regulates various cellular processes through its chromatin remodeling activity, and especially the regulatory role of SMARCAD1^Fun30 in gene expression control, maintenance and establishment of heterochromatin, and DNA damage repair. Moreover, we review the studies on the molecular mechanism of SMARCAD1^Fun30 that promotes the DNA end-resection on double-strand break ends, including the mechanisms of recruitment, activity regulation and chromatin remodeling.

Keywords: DNA damage; DNA end-resection; SMARCAD1/Fun30; chromatin remodeler; post-translational modification; single-stranded DNA.

Publication types

Review