Escherichia coli cells defective for the recN gene display constitutive elevation of mutagenesis at 3,N(4)-ethenocytosine via an SOS-induced mechanism.
Escherichia coli cells defective for the recN gene display constitutive elevation of mutagenesis at 3,N(4)-ethenocytosine via an SOS-induced mechanism.
复制标题
存在recN基因缺陷的大肠杆菌细胞通过SOS诱导的机制表现出3,N(4)-乙烯胞嘧啶诱变的组成性升高。
DOI：
10.1046/j.1365-2958.2000.02045.x
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发表时间：
2000
影响因子：
3.6
通讯作者：
Humayun,MZ
中科院分区：
文献类型：
--
作者：
Dunman,PM;Ren,L;Rahman,MS;Palejwala,VA;Murphy,HS;Volkert,MR;Humayun,MZ
大肠杆菌UVM（紫外线诱变调制）反应是一种DNA损伤诱导的诱变途径，在转染的单链M13载体DNA上的3，N4-乙烯胞嘧啶（εC）损伤处检测到显著增加的诱变。所有主要类型的DNA损伤剂都可以诱导UVM，并且这种现象与先前在E中表征的致突变反应无关。杆菌为了进一步理解这一现象，我们着手鉴定和表征UVM反应中的突变体。筛选1-甲基-3-硝基-1-亚硝基胍诱导基因缺陷的突变体细胞库发现，recN基因的缺陷导致εC残基突变的组成性升高。与正常细胞在εC损伤处显示约60%的诱变，但在UVM诱导后显示约60%的诱变相反，recN缺陷菌株在未处理细胞中的εC损伤位点显示约50%的诱变。 然而，recN介导的诱变反应被发现需要recA基因和umuDC基因，并且可以在含有SOS转录抑制因子莱克萨的质粒存在下被抑制。这些结果意味着recN细胞对于SOS突变功能具有组成性活性。εC诱变在recN细胞中增强的观察结果证实了先前的发现，即εC处的诱变也可以通过SOS途径独立地升高。
TheEscherichia coliUVM (UV Modulation of mutagenesis) response is a DNA damage‐inducible mutagenic pathway detected as significantly increased mutagenesis at 3,N4‐ethenocytosine (εC) lesions borne on transfected single‐stranded M13 vector DNA. All major classes of DNA‐damaging agents can induce UVM, and the phenomenon is independent of previously characterized mutagenic responses inE. coli. To understand this phenomenon further, we set out to identify and characterize mutants in the UVM response. Screening a mutant bank of cells defective for 1‐methyl‐3‐nitro‐1‐nitrosoguanidine‐inducible genes revealed that defects in therecNgene cause a constitutive elevation of mutagenesis at εC residues. In contrast to normal cells that show ≈ 6% mutagenesis at εC lesions, but ≈ 60% upon UVM induction,recN‐defective strains display approximately 50% mutagenesis at εC lesion sites in untreated cells. However, therecN‐mediated mutagenesis response was found to require therecAgene and theumuDCgenes, and could be suppressed in the presence of a plasmid harbouring the SOS transcriptional repressor LexA. These results imply thatrecNcells are constitutively active for SOS mutagenesis functions. The observation that εC mutagenesis is enhanced inrecNcells confirms previous findings that mutagenesis at εC can also be independently elevated by the SOS pathway.