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The Ino80 chromatin-remodeling complex restores chromatin structure during UV DNA damage repair.

机译:Ino80染色质重塑复合物可在UV DNA损伤修复过程中恢复染色质结构。

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摘要

Chromatin structure is modulated during deoxyribonucleic acid excision repair, but how this is achieved is unclear. Loss of the yeast Ino80 chromatin-remodeling complex (Ino80-C) moderately sensitizes cells to ultraviolet (UV) light. In this paper, we show that INO80 acts in the same genetic pathway as nucleotide excision repair (NER) and that the Ino80-C contributes to efficient UV photoproduct removal in a region of high nucleosome occupancy. Moreover, Ino80 interacts with the early NER damage recognition complex Rad4-Rad23 and is recruited to chromatin by Rad4 in a UV damage-dependent manner. Using a modified chromatin immunoprecipitation assay, we find that chromatin disruption during UV lesion repair is normal, whereas the restoration of nucleosome structure is defective in ino80 mutant cells. Collectively, our work suggests that Ino80 is recruited to sites of UV lesion repair through interactions with the NER apparatus and is required for the restoration of chromatin structure after repair.
机译:脱氧核糖核酸切除修复过程中染色质结构被调节,但如何实现尚不清楚。酵母Ino80染色质重塑复合物(Ino80-C)的丢失会中等程度地使细胞对紫外线(UV)敏感。在本文中,我们表明INO80与核苷酸切除修复(NER)的遗传途径相同,并且Ino80-C有助于在高核小体占用区域中有效去除UV光产物。此外,Ino80与早期的NER损伤识别复合物Rad4-Rad23相互作用,并通过Rad4以依赖于UV损伤的方式被募集到染色质上。使用改良的染色质免疫沉淀测定法,我们发现紫外线损伤修复期间的染色质破坏是正常的,而ino80突变细胞中核小体结构的恢复是有缺陷的。总的来说,我们的工作表明,Ino80通过与NER仪器的相互作用而被募集到UV损伤修复部位,并且是修复后恢复染色质结构所必需的。

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