摘要
对本实验室构建的错配修复功能缺陷细胞HeLa-MLH1-的次黄嘌呤鸟嘌呤磷酸核糖基转移酶(hprt)基因自发突变率进行检测,发现相对于无hMLH1缺陷的对照细胞HeLa-R9和HeLa而言,其突变率分别提高了878倍和353倍(P<001),此表型改变与本实验室已构建的另一错配修复功能缺陷细胞HeLa-MSH2-相同。本实验室还证明HeLa-MLH1-细胞存在甲基硝基亚硝基胍(methylnitronitrosoguanidine,MNNG)耐受,这与我们在HeLa-MSH2-细胞实验中的发现不同,提示不同的错配修复基因功能缺陷对细胞表型影响不尽相同。
Spontaneous mutation rate at hypoxanthine phosphoribosyltransferase (hprt) locus increased markedly in HelaMLH1 - cell, mismatch repair (MMR) deficient cell line, it exhibited a 8.78 and 3.53fold increase in mutation frequency relative to MMRproficient HeLaR9 and HeLa cell line. This phenotype is similar to another mismatch repair defective cell line HeLaMSH2 -. MNNG tolerance also appeared in HeLaMLH1 -cell but no MNNG tolerance in HeLaMSH2 - cell. These data suggest that different MMR gene defect exerts different effects on mutator phenotypes.
出处
《癌变.畸变.突变》
CAS
CSCD
1998年第4期203-206,共4页
Carcinogenesis,Teratogenesis & Mutagenesis
关键词
HeLa-MLH1^-
细胞实验
生物学特性
突变
DNArepair
hypoxanthine phosphoribosyltransferase
mutation
methylnitronitrosoguanidine