Nara K, Nagashima F, Yasui A
Department of Molecular Genetics, Institute of Development, Aging and Cancer, Medical Faculty, Tohoku University, Sendai, Japan.
Cancer Res. 2001 Jan 1;61(1):50-2.
We have isolated N-methyl-N'-nitro-N-nitrosoguanidine-resistant cell lines from 43-3B Chinese hamster ovary cells, which are deficient in the ERCC1 gene involved in nucleotide excision repair. By Western blotting analysis, we found cell lines that are deficient or decreased in the amount of MSH6, or PMS2, or MSH2 proteins. Cell extracts of these cell lines show reduced efficiency of G:T mismatch repair activity. Compared with 43-3B, these cell lines exhibit highly elevated UV-induced mutation rates, indicating that mammalian mismatch repair can suppress UV-induced mutagenesis and may play a role in the fidelity of DNA replication at the sites of UV damage.
我们从43-3B中国仓鼠卵巢细胞中分离出了对N-甲基-N'-硝基-N-亚硝基胍具有抗性的细胞系，这些细胞缺乏参与核苷酸切除修复的ERCC1基因。通过蛋白质免疫印迹分析，我们发现了一些细胞系，它们的MSH6、PMS2或MSH2蛋白数量不足或减少。这些细胞系的细胞提取物显示G:T错配修复活性效率降低。与43-3B细胞系相比，这些细胞系表现出紫外线诱导的突变率大幅升高，这表明哺乳动物错配修复可以抑制紫外线诱导的诱变作用，并且可能在紫外线损伤部位的DNA复制保真度方面发挥作用。
