Koehler D R, Hanawalt P C
Department of Biological Sciences, Stanford University, CA 94305-5020, USA.
Nucleic Acids Res. 1996 Aug 1;24(15):2877-84. doi: 10.1093/nar/24.15.2877.
We examined the relationship between the nuclear matrix and DNA in the dihydrofolate reductase domain following irradiation of Chinese hamster cells with UV light. The fraction of matrix-bound DNA increased in transcribed and non-transcribed regions during a 3 h period after irradiation. However, no increase was observed with excision repair-deficient cells mutant for the ERCC1 gene. The major UV-induced lesion, the cyclobutane pyrimidine dimer, increased in frequency in the matrix-bound DNA 1 h after irradiation, in both transcribed and non-transcribed regions, but decreased subsequently. This phenomenon was also lacking in excision repair-deficient cells. These data demonstrate that recruitment of lesion-containing DNA to the nuclear matrix occurs following UV irradiation and suggest that this recruitment is dependent upon nucleotide excision repair. This is consistent with the concept of a 'repair factory' residing on the nuclear matrix at which excision repair occurs.
在用紫外线照射中国仓鼠细胞后,我们研究了二氢叶酸还原酶结构域中核基质与DNA之间的关系。照射后3小时内,转录区和非转录区中与基质结合的DNA比例增加。然而,对于ERCC1基因缺失的切除修复缺陷细胞,未观察到这种增加。主要的紫外线诱导损伤——环丁烷嘧啶二聚体,在照射后1小时,在转录区和非转录区的与基质结合的DNA中频率均增加,但随后下降。这种现象在切除修复缺陷细胞中也不存在。这些数据表明,紫外线照射后含损伤的DNA会募集到核基质上,并且表明这种募集依赖于核苷酸切除修复。这与存在于核基质上发生切除修复的“修复工厂”概念相一致。