Abstract
Cells are constantly damaged by factors that can induce DNA damage. Eukaryotic cells must rapidly load DNA repair proteins onto damaged chromatin during the DNA damage response (DDR). Chromatin-remodeling complexes use the energy from ATP hydrolysis to remodel nucleosomes and have well-established functions in transcription. Emerging lines of evidence indicate that chromatin-remodeling complexes are important and may remodel nucleosomes during DNA damage repair. New studies also reveal that ATP-dependent chromatin remodeling is involved in cell cycle progression, signal transduction pathways, and interaction and modification of DDR-related proteins that are specifically and intimately connected with the process of DNA damage. This article summarizes the recent advances in our understanding of the interplay between chromatin remodeling and DNA damage response.
Highlights
Cells from yeast to mammals are constantly damaged by different factors [1]
We examine the recent advances in elucidating how chromatin-remodeling factors are recruited to double strand breaks (DSBs) sites and function directly in response to DNA damage response (DDR) signals
These findings indicate a complex role for cohesin in gene expression and DNA repair, especially during G2/M phase
Summary
Cells from yeast to mammals are constantly damaged by different factors [1]. Chromatin-remodeling factors are highly conserved, and the modification of chromatin structure during the DNA damage response (DDR) is common to yeast, Droshophila, mice and humans. Numerous chromatin-remodeling factors, especially those from the INO80 and SWI2 subfamilies, are recruited to double strand breaks (DSBs) in response to DDR. Environmental stress, such as ionizing radiation, and endogenous events, such as replication fork collapse and antigen receptor gene rearrangement, can all induce DSBs. In response to DSB lesions, cells rapidly activate a dedicated signal transduction network to convey the damage signal to many types of cellular machinery that are involved in different processes, including transcriptional regulation, cell cycle regulation, apoptosis and DNA repair. We examine the recent advances in elucidating how chromatin-remodeling factors are recruited to DSB sites and function directly in response to DDR signals
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