Thoma Fritz
Institut für Zellbiologie, ETH-Hönggerberg, CH-8093 Zürich, Switzerland.
DNA Repair (Amst). 2005 Jul 28;4(8):855-69. doi: 10.1016/j.dnarep.2005.04.005.
Nucleotide excision repair and reversal of pyrimidine dimers by photolyase (photoreactivation) are two major pathways to remove UV-lesions from DNA. Here, it is discussed how lesions are recognized and removed when the DNA is condensed into nucleosomes. During the recent years it was shown that nucleosomes inhibit photolyase and excision repair in vitro and slow down repair in vivo. The correlation of DNA-repair rates with nucleosome positions in yeast suggests that intrinsic properties of nucleosomes such as mobility and transient unwrapping of nucleosomal DNA facilitate damage recognition. Moreover, it was shown that nucleosome remodeling activities can act on UV-damaged DNA in vitro and facilitate repair suggesting that random remodeling of chromatin might contribute to damage recognition in vivo. Recent work on nucleosome structure and mobility is included to evaluate how nucleosomes accommodate DNA lesions and how nucleosome mobility and remodeling can take place on damaged DNA.
核苷酸切除修复以及通过光裂合酶逆转嘧啶二聚体（光复活作用）是从DNA中去除紫外线损伤的两条主要途径。本文讨论了DNA浓缩成核小体时损伤是如何被识别和去除的。近年来研究表明，核小体在体外抑制光裂合酶和切除修复，并在体内减缓修复过程。酵母中DNA修复率与核小体位置的相关性表明，核小体的内在特性，如核小体DNA的流动性和瞬时解旋，有助于损伤识别。此外，研究表明核小体重塑活性在体外可作用于紫外线损伤的DNA并促进修复，这表明染色质的随机重塑可能有助于体内的损伤识别。本文纳入了近期关于核小体结构和流动性的研究工作，以评估核小体如何容纳DNA损伤，以及核小体的流动性和重塑如何在受损DNA上发生。
