Recombinational repair is critical for survival of Escherichia coli exposed to nitric oxide.
Recombinational repair is critical for survival of Escherichia coli exposed to nitric oxide.
复制标题
重组修复对于暴露于一氧化氮的大肠杆菌的生存至关重要。
DOI：
10.1128/jb.183.1.131-138.2001
复制
发表时间：
2001
影响因子：
3.2
通讯作者：
Engelward,BP
中科院分区：
文献类型：
--
作者：
Spek,EJ;Wright,TL;Stitt,MS;Taghizadeh,NR;Tannenbaum,SR;Marinus,MG;Engelward,BP
一氧化氮（NO⋅）对许多生物过程至关重要，包括信号转导和巨噬细胞介导的免疫。在本研究中，我们探讨了NO⋅诱导的大肠杆菌DNA损伤的生物学效应。测定碱基切除修复、核苷酸切除修复（NER）和重组修复在预防NO⋅⋅毒性中的相对重要性。缺乏NER或DNA糖基酶的大肠杆菌（包括修复烷基化损伤[alkA tagstrain]，氧化损伤[fpg nei nthstrain]和脱氨胞嘧啶[ungstrain]的大肠杆菌）基本上显示出野生型的NO⋅抗性水平。然而，apyrimidinic/apurinic （xth）内切酶缺陷细胞（第xth菌株）对NO⋅杀伤非常敏感，这表明基础位点的正常加工对于防御NO⋅至关重要。此外，突变细胞对NO⋅诱导的杀伤非常敏感。SOS-deficient （lexA3）和Holliday junction resolvase-deficient （ruvC）细胞对NO⋅都非常敏感，说明SOS和重组修复在抵御NO⋅中起重要作用。此外，特异性缺乏双链末端修复的菌株（recbcd菌株）对NO⋅非常敏感，这表明NO⋅暴露导致双链末端的形成。这些双链末端的一个结果是NO⋅诱导基因工程底物的同源重组。综上所述，现在很清楚，除了已知的NO⋅诱变效应外，考虑NO⋅诱导的遗传变化谱中的重组事件也很重要。此外，重组修复对NO⋅暴露细胞存活的重要性揭示了入侵微生物的潜在易感性因素。
Nitric oxide (NO⋅) is critical to numerous biological processes, including signal transduction and macrophage-mediated immunity. In this study, we have explored the biological effects of NO⋅-induced DNA damage onEscherichia coli. The relative importance of base excision repair, nucleotide excision repair (NER), and recombinational repair in preventing NO⋅-induced toxicity was determined.E. colistrains lacking either NER or DNA glycosylases (including those that repair alkylation damage [alkA tagstrain], oxidative damage [fpg nei nthstrain], and deaminated cytosine [ungstrain]) showed essentially wild-type levels of NO⋅resistance. However, apyrimidinic/apurinic (AP) endonuclease-deficient cells (xth nfostrain) were very sensitive to killing by NO⋅, which indicates that normal processing of abasic sites is critical for defense against NO⋅. In addition,recAmutant cells were exquisitely sensitive to NO⋅-induced killing. Both SOS-deficient (lexA3) and Holliday junction resolvase-deficient (ruvC) cells were very sensitive to NO⋅, indicating that both SOS and recombinational repair play important roles in defense against NO⋅. Furthermore, strains specifically lacking double-strand end repair (recBCDstrains) were very sensitive to NO⋅, which suggests that NO⋅exposure leads to the formation of double-strand ends. One consequence of these double-strand ends is that NO⋅induces homologous recombination at a genetically engineered substrate. Taken together, it is now clear that, in addition to the known point mutagenic effects of NO⋅, it is also important to consider recombination events among the spectrum of genetic changes that NO⋅can induce. Furthermore, the importance of recombinational repair for cellular survival of NO⋅exposure reveals a potential susceptibility factor for invading microbes.