通过G.C-T.A颠换实现大肠杆菌trpA23错义突变的自发和苯并[a]芘诱导回复需要MucA蛋白的加工：MutY DNA糖基化酶缺陷的影响

Processing of MucA protein is required for spontaneous and benzo[a]pyrene-induced reversion of the Escherichia coli trpA23 missense mutation by G.C-T.A transversions: effect of a deficiency in the MutY DNA glycosylase.

作者信息

Urios A, Herrera G, Aleixandre V, Blanco M

机构信息

Instituto de Investigaciones Citológicas, Fundación Valenciana de Investigaciones Biomédicas, Spain.

出版信息

Mutat Res. 1994 Dec 1;311(2):257-63. doi: 10.1016/0027-5107(94)90184-8.

DOI:10.1016/0027-5107(94)90184-8

Abstract

We have studied the influence of the processing of MucA protein on the occurrence of base substitution mutations. Escherichia coli strains carrying the trpA23 missense mutation and having a full deletion of the chromosomal umuD/C operon were transformed with plasmids encoding the MucB protein together with either wild-type MucA or the nonprocessable MucA202 protein. The efficient reversion of the trpA23 allele by G.C-T.A transversions in benzo[a]pyrene (B[a]P)-treated cells required the function of a matured MucA protein. This processed protein was also necessary for the occurrence of G.C-T.A transversions targeted at spontaneous DNA lesions and for the SOS mutator effect dependent on the constitutive coprotease activity of the RecA730 protein. In contrast, G.C-T.A transversions reverting trpA23 were spontaneously generated by an SOS-independent mechanism in cells deficient in the MutY DNA glycosylase.

摘要

我们研究了MucA蛋白的加工过程对碱基取代突变发生的影响。携带trpA23错义突变且染色体umuD/C操纵子完全缺失的大肠杆菌菌株，用编码MucB蛋白以及野生型MucA或不可加工的MucA202蛋白的质粒进行转化。在经苯并[a]芘（B[a]P）处理的细胞中，trpA23等位基因通过G.C-T.A颠换实现高效回复突变需要成熟MucA蛋白的功能。这种加工后的蛋白对于针对自发DNA损伤的G.C-T.A颠换的发生以及依赖RecA730蛋白组成型共蛋白酶活性的SOS诱变效应也是必需的。相比之下，在缺乏MutY DNA糖基化酶的细胞中，回复trpA23的G.C-T.A颠换是通过一种不依赖SOS的机制自发产生的。