Abstract
CCCTC-binding factor (CTCF) plays an essential role in regulating the structure of chromatin by binding DNA strands for defining the boundary between active and heterochromatic DNA. However, the role of CTCF in DNA damage response remains elusive. Here, we show that CTCF is quickly recruited to the sites of DNA damage. The fast recruitment is mediated by the zinc finger domain and poly (ADP-ribose) (PAR). Further analyses show that only three zinc finger motifs are essential for PAR recognition. Moreover, CTCF-deficient cells are hypersensitive to genotoxic stress such as ionizing radiation (IR). Taken together, these results suggest that CTCF participate in DNA damage response via poly(ADP-ribosylation).
Highlights
Chromatin is dynamically regulated to higher order structures[1,2]
To investigate whether CTCF participates in DNA damage response, we ask if CTCF is recruited to the sites of DNA damage
The GFP-CTCF was expressed in U2OS cells with lower expression level compared to the endogenous level of CTCF, and the cells were treated with laser microirradiation to induced DNA lesions
Summary
Chromatin is dynamically regulated to higher order structures[1,2]. In response to DNA damage, a proper chromatin state is formed for facilitating DNA repair. Over the past few years, many PAR-binding motifs have been identified, including the PBZ, MACRO, BRCT, FHA, RRM, OB-fold, PIN domains, in various DNA damage response factors[11,14,18,19,20,21]. This early and fast wave of the recruitment brings DNA damage response factors to the proximity of DNA lesions. Recent studies show that CTCF regulates three-dimensional structure of the chromatin fiber in the nucleus, based on its ability to mediate interactions between distant sequences[23,27,28]. Our study provides a novel regulation mechanism in DNA damage response
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