Boshoff H I, Durbach S I, Mizrahi V
MRC/SAIMR/WITS Molecular Mycobacteriology Research Unit, South African Institute for Medical Research and Department of Haematology & Molecular Medicine, University of the Witwatersrand, Johannesburg.
Scand J Infect Dis. 2001;33(2):101-5. doi: 10.1080/003655401750065463.
In this paper, we review the evidence supporting the notion that the genome of Mycobacterium tuberculosis sustains considerable damage as a result of exposure to nitrosative and oxidative stress. On these grounds, we propose a model in which stress-induced DNA damage in M. tuberculosis plays a role in the evolution of chromosomally encoded drug resistance mutations by altering the global mutation rate by mechanisms akin to SOS mutagenesis. Finally we review some of the factors determining the evolution of PE/PPE and MIRU (There are many abbreviations in this paper which are not defined, e.g. SOS, PE/PPE and MIRU. Please indicate whether these are well known and will be understood by readers or whether they should be defined at first mention) loci whose sequence characteristics are suggestive of their classification as heritable local mutators.
在本文中，我们回顾了支持以下观点的证据：结核分枝杆菌的基因组因暴露于亚硝化和氧化应激而遭受相当大的损伤。基于这些理由，我们提出了一个模型，其中结核分枝杆菌中应激诱导的DNA损伤通过类似于SOS诱变的机制改变全局突变率，在染色体编码的耐药性突变的进化中发挥作用。最后，我们回顾了一些决定PE/PPE和MIRU（本文中有许多未定义的缩写，例如SOS、PE/PPE和MIRU。请指出这些缩写是否为读者所熟知并能理解，或者是否应在首次提及时进行定义）位点进化的因素，其序列特征表明它们可被归类为可遗传的局部诱变剂。
