SlyA regulates virulence gene expressions through activation of pchA regulatory gene in enterohemorrhagic Escherichia coli
SlyA regulates virulence gene expressions through activation of pchA regulatory gene in enterohemorrhagic Escherichia coli
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SlyA通过激活肠出血性大肠杆菌中的pchA调节基因来调节毒力基因表达
DOI：
10.1111/1348-0421.13027
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
Tobe T
中科院分区：
文献类型：
--
作者：
Hamamura R;Yen H;Tobe T
SlyA是一种DNA结合蛋白，可改变由组蛋白样类核结构蛋白（H-NS）组成的类核复合物并激活基因表达。在肠出血性大肠杆菌（EHEC）中，毒力基因的表达被H-NS抑制，但通过释放类核复合物来响应环境因素而上调。本研究检查了EHEC中slyA缺失突变的影响，发现与野生型相比，突变体中肠上皮细胞消失（LEE）位点编码的EspB和Tir的产生以及细胞粘附能力降低。LEE 1操纵子的启动子活性，包括调节基因ler，通过突变降低，但是启动子控制的LEE 1调节基因pchA的表达，消除了这种作用。pchA基因启动子活性被lyA突变下调。此外，编码区是其调控所必需的，并与SlyA结合，这表明SlyA直接调控pchA。然而，theslyA突变并不影响丁酸诱导的pchA启动子活性的增加。此外，pchA启动子活性增加，通过诱导flrp，丁酸反应的调节基因，在theslyA突变体，相反，通过引入高拷贝的slyA到thelrp突变体。这些结果表明，SlyA是pchA的正调节剂，并且独立于Lrp调节系统。SlyA可能参与了EHEC的毒力表达，在没有丁酸反应的情况下维持一定的表达水平。
SlyA is a DNA‐binding protein that alters the nucleoid complex composed of histone‐like nucleoid‐structuring protein (H‐NS) and activates gene expression. In enterohemorrhagicEscherichia coli(EHEC), the expression of virulence genes is repressed by H‐NS but is up‐regulated in response to environmental factors by releasing a nucleoid complex. This study examined the effect ofslyAdeletion mutation in EHEC and discovered that the production of the locus of enterocyte effacement (LEE)‐encoded EspB and Tir, as well as the cell adherence ability, was reduced in the mutant compared with the wild type. The promoter activity of theLEE1operon, including the regulatory gene,ler, was reduced byslyAmutation, buttacpromoter‐controlled expression ofpchA, which is a regulatory gene ofLEE1, abolished the effect. The promoter activity ofpchAwas down‐regulated by theslyAmutation. Furthermore, the coding region was required for its regulation and was bound to SlyA, which indicates the direct regulation ofpchAby SlyA. However, theslyAmutation did not affect the butyrate‐induced increase inpchApromoter activity. Additionally, thepchApromoter activity was increased via induction oflrp, a regulatory gene for butyrate response, in theslyAmutant and, conversely, by introducing high copies ofslyAinto thelrpmutant. These results indicate that SlyA is a positive regulator ofpchAand is independent of the Lrp regulatory system. SlyA may be involved in the virulence expression in EHEC, maintaining a certain level of expression in the absence of a butyrate response.