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N-甲基-N'-硝基-N-亚硝基胍对中国仓鼠卵巢细胞和大肠杆菌细胞染色体上gpt基因的诱变特异性。

Mutagenic specificity of N-methyl-N'-nitro-N-nitrosoguanidine in the gpt gene on a chromosome of Chinese hamster ovary cells and of Escherichia coli cells.

作者信息

Sockett H, Romac S, Hutchinson F

机构信息

Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06511.

出版信息

Mol Gen Genet. 1991 Jun;227(2):252-9. doi: 10.1007/BF00259678.

Abstract

DNA base sequence changes induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) mutagenesis have been determined for the Escherichia coli gpt gene stably incorporated in a chromosome of Chinese hamster ovary cells and in the chromosome of both growing and starving E. coli cells, instead of on a plasmid as in most previous studies. In the three cases, nearly all mutations were G:C to A:T transitions, with a 2- to 4-fold higher mutation rate, compared to other sites, at guanines flanked on the 5' side by another guanine. Mutagenic hot spots in these experiments were less prominent than in published results for MNNG mutagenesis of gpt and of other genes. A suggested explanation involves repair of O6meG. At low levels of mutagenic products, most are repaired and even small differences in the repair rates leads to large differences in the relative amounts of residual O6meG at various sites; in contrast, at high levels of mutagenic products there is little effect of repair on the distribution.

摘要

已确定由N-甲基-N'-硝基-N-亚硝基胍(MNNG)诱变诱导的DNA碱基序列变化,这些变化针对稳定整合在中国仓鼠卵巢细胞染色体以及生长和饥饿的大肠杆菌细胞染色体中的大肠杆菌gpt基因,而非如大多数先前研究那样在质粒上。在这三种情况下,几乎所有突变都是G:C到A:T的转换,与其他位点相比,在5'侧被另一个鸟嘌呤侧翼的鸟嘌呤处,突变率高出2至4倍。这些实验中的诱变热点不如已发表的关于gpt和其他基因的MNNG诱变结果中那么突出。一种可能的解释涉及O6meG的修复。在诱变产物水平较低时,大多数会被修复,即使修复率的微小差异也会导致不同位点残留O6meG相对量的巨大差异;相反,在诱变产物水平较高时,修复对分布几乎没有影响。

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