Parrish D D, Feng X, Lambert M W
Department of Laboratory Medicine and Pathology, UMDNJ, New Jersey Medical School, Newark 07103.
Biochem Biophys Res Commun. 1992 Dec 15;189(2):782-9. doi: 10.1016/0006-291x(92)92270-8.
A DNA endonuclease complex which recognizes predominantly pyrimidine dimers in UVC irradiated DNA has been isolated from the chromatin of normal human and xeroderma pigmentosum, complementation group D (XPD) lymphoblastoid cells. The activity of the normal complex on UVC irradiated DNA was increased approximately 2.5 and 1.5 fold over activity on damaged naked DNA, when core (histones H2A, H2B, H3, H4) and total (core+histone H1) nucleosomal DNA, respectively, was used. In contrast, the XPD complex showed no increase in activity on UVC irradiated total and only a 1.4 fold increase on UVC irradiated core nucleosomal DNA, indicating that the XPD complex is defective in its ability to incise UVC irradiated nucleosomal DNA. The normal complex was able to correct this defect in the XPD complex at the nucleosomal level.
一种主要识别经紫外线C（UVC）照射的DNA中嘧啶二聚体的DNA核酸内切酶复合物已从正常人及着色性干皮病互补组D（XPD）淋巴母细胞的染色质中分离出来。当分别使用核心（组蛋白H2A、H2B、H3、H4）和完整（核心+组蛋白H1）核小体DNA时，正常复合物对经UVC照射的DNA的活性比其对受损裸DNA的活性分别提高了约2.5倍和1.5倍。相比之下，XPD复合物对经UVC照射的完整核小体DNA的活性没有增加，对经UVC照射的核心核小体DNA的活性仅增加了1.4倍，这表明XPD复合物在切割经UVC照射的核小体DNA的能力上存在缺陷。正常复合物能够在核小体水平上纠正XPD复合物的这一缺陷。
