Escherichia coli gene expression responsive to levels of the response regulator EvgA
Escherichia coli gene expression responsive to levels of the response regulator EvgA
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DOI：
10.1128/jb.184.22.6225-6234.2002
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发表时间：
2002-11-01
影响因子：
3.2
通讯作者：
Church, GM
中科院分区：
文献类型：
--
作者：
Masuda, N;Church, GM
为了研究 EvgA 反应调节因子的功能，我们通过寡核苷酸微阵列比较了 EvgA 过表达和 EvgA 缺乏的大肠杆菌菌株的全基因组转录谱。微阵列测量鉴定出至少 37 个 EvgA 激活基因，包括耐酸相关基因 gadABC 和 hdeAB、外排泵基因 yhiUV 和 emrK，以及 21 个功能未知的基因。 EvgA 过度表达赋予指数生长细胞耐酸性。这种酸性耐受性通过删除 ydeP、ydeO 或 yhiE 来消除，这是由 EvgA 过表达诱导的。这些结果表明 ydeP、ydeO 和 yhiE 是与耐酸性相关的新基因，并且 EvgA 调节多个耐酸性基因。此外，yhiE 的缺失完全消除了稳定期细胞的耐酸性，表明 YhiE 在稳定期耐酸性中发挥着关键作用。 acrB 缺失突变体中由 EvgA 过表达引起的多药耐药性通过 yhiUV 的缺失而被完全消除，而 emrKY 缺失对 EvgA 过表达引起的耐药性增加没有影响。此外，EvgA 过表达不会赋予 tolC 缺陷菌株抗性。这些结果表明，EvgA 过表达诱导的 YhiUV 在功能上与 TolC 相关，并有助于多药耐药性。
To investigate the function of the EvgA response regulator, we compared the genome-wide transcription profile of EvgA-overexpressing and EvgA-lacking Escherichia coli strains by oligonucleotide microarrays. The microarray measurements allowed the identification of at least 37 EvgA-activated genes, including acid resistance-related genes gadABC and hdeAB, efflux pump genes yhiUV and emrK, and 21 genes with unknown function. EvgA overexpression conferred acid resistance to exponentially growing cells. This acid resistance was abolished by deletion of ydeP, ydeO, or yhiE, which was induced by EvgA overexpression. These results suggest that ydeP,ydeO, and yhiE are novel genes related to acid resistance and that EvgA regulates several acid resistance genes. Furthermore, the deletion of yhiE completely abolished acid resistance in stationary-phase cells, suggesting that YhiE plays a critical role in stationary-phase acid resistance. The multidrug resistance in an acrB deletion mutant caused by EvgA overexpression was completely abolished by deletion of yhiUV, while the emrKY deletion had no effect on the increase in resistance by EvgA overexpression. In addition, EvgA overexpression did not confer resistance in a tolC-deficient strain. These results suggest that YhiUV induced by EvgA overexpression is functionally associated with TolC and contributes to multidrug resistance.