Participation of Rho-dependent transcription termination in oxidative stress sensitivity caused by an rpoB mutation
Participation of Rho-dependent transcription termination in oxidative stress sensitivity caused by an rpoB mutation
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DOI：
10.1111/j.1365-2443.2005.00849.x
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发表时间：
2005-05-01
期刊：
影响因子：
2.1
通讯作者：
Sekimizu, K
中科院分区：
文献类型：
--
作者：
Kawamura, N;Kurokawa, K;Sekimizu, K
转录终止过程对基因表达调控的作用知之甚少。无论是一个多拷贝供应的rof基因或双环霉素，这两个抑制转录终止Rho因子，抑制了增加的敏感性，在大肠杆菌中的利福平耐药rpoB突变的氧化应激。rnk基因的多拷贝供应也抑制了氧化应激敏感性，与突变细胞中三磷酸核苷浓度降低的恢复一致，这是影响体外转录终止效率的因素之一。因此，一个适当的，非过度终止频率在Rho依赖的转录终止子可能有助于氧化应激生存。并对氧化应激在耐药菌中的临床应用进行了讨论。
The role of transcription termination process for gene expression regulation is poorly understood. Either a multicopy supply of the rof gene or bicyclomycin, both of which inhibit the transcription termination Rho factor, suppressed the increased sensitivity to oxidative stress of the rifampicin-resistant rpoB mutation in Escherichia coli. Multi-copy supply of the rnk gene also suppressed oxidative stress sensitivity, coincident with the recovery of the reduced concentration of nucleoside triphosphates in the mutant cells, which is one of the factors that affects transcription termination efficiency in vitro. Thus, an appropriate, nonexcessive termination frequency at Rho-dependent transcription terminators might contribute to oxidative stress survival. Clinical application of oxidative stress against drug resistant bacteria is also discussed.