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首页> 外文期刊>Cell cycle >The chromatin remodeling factor BRG1 stimulates nucleotide excision repair by facilitating recruitment of XPC to sites of DNA damage.
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The chromatin remodeling factor BRG1 stimulates nucleotide excision repair by facilitating recruitment of XPC to sites of DNA damage.

机译：染色质重塑因子BRG1通过促进XPC募集到DNA损伤部位来刺激核苷酸切除修复。

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摘要

BRGI is a catalytic subunit of the human SWI/SNF-like BAF chromatin remodeling complexes. Recent findings have shown that inactivation of BRGI sensitizes mammalian cells to various DNA damaging agents, including ultraviolet (UV) and ionizing radiation. However, it is unclear whether BRGI facilitates nucleotide excision repair (NER). Here we show that re-expression of BRGI in cells lacking endogenous BRGI expression stimulates nucleotide excision repair of UV induced DNA damage. Using a micropore UV radiation technique, we demonstrate that recruitment of the DNA damage recognition protein XPC to sites of UV lesions is disrupted when BRGI is stably depleted. Chromatin immunoprecipitation of the endogenous DDB2 protein, which is involved in recruiting XPC to UV-induced CPDs (cyclobutane pyrimidine dimers), shows that elevated levels of BRGI are associated with DDB2 in chromatin in response to UV radiation. Additionally, we detected slow BRGI accumulation at sites of UV lesions. Our findings suggest that the chromatin remodeling factor BRGI is recruited to sites of UV lesions to facilitate NER in human chromatin.
机译：BRGI是人类SWI / SNF样BAF染色质重塑复合物的催化亚基。最近的发现表明，BRGI的失活使哺乳动物细胞对各种DNA破坏剂敏感，包括紫外线（UV）和电离辐射。但是，尚不清楚BRGI是否促进核苷酸切除修复（NER）。在这里，我们表明在缺乏内源性BRGI表达的细胞中BRGI的重新表达刺激了紫外线诱导的DNA损伤的核苷酸切除修复。使用微孔紫外线辐射技术，我们证明了当BRGI稳定耗尽时，DNA损伤识别蛋白XPC募集到UV损伤的部位被破坏了。内源性DDB2蛋白的染色质免疫沉淀涉及将XPC募集到UV诱导的CPD（环丁烷嘧啶二聚体）中，表明BRGI的水平升高与染色质中的DDB2有关。此外，我们检测到BRGI在UV损伤部位的积累缓慢。我们的发现表明，染色质重塑因子BRGI被募集到UV损伤部位，以促进人类染色质中的NER。

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