Global transcriptional regulation by H-NS and its biological influence on the virulence of Enterohemorrhagic Escherichia coli.
Global transcriptional regulation by H-NS and its biological influence on the virulence of Enterohemorrhagic Escherichia coli.
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DOI：
10.1016/j.gene.2016.05.007
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发表时间：
2016-08
期刊：
影响因子：
3.5
通讯作者：
Baoshan Wan;Qiufen Zhang;Jing Tao;Aiping Zhou;Yu-Feng Yao;Jin-jing Ni
中科院分区：
文献类型：
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作者：
Baoshan Wan;Qiufen Zhang;Jing Tao;Aiping Zhou;Yu-Feng Yao;Jin-jing Ni
H-NS作为一种全局性转录调节因子，在细菌中发挥着广泛的生物学作用。为了明确H-NS在大肠杆菌（EHEC）基因转录调控中的作用，进一步探讨H-NS蛋白的生物学意义，我们对突变体进行了转录组分析。共鉴定出983个基因受H-NS的调控。缺失突变体中分别有213个基因表达下调和770个基因表达上调。有趣的是，毒力质粒pO 157上的97个基因中有34个被H-NS下调。与野生型相比，hns缺失突变株在巨噬细胞中的存活率降低，但在小鼠肠道的定植能力增强，对BALB/c小鼠的毒力增强。与感染野生型菌株的BALB/c小鼠相比，感染缺失突变株的BALB/c小鼠的存活率较低，肠道细菌负荷较高，特别是当肠道微生物群不受抗生素给药干扰时。这些结果表明，H-NS通过与宿主肠道菌群相互作用在EHEC的毒力中起重要作用。
As a global transcriptional regulator, H-NS, the histone-like nucleoid-associated DNA-binding and bridging protein, plays a wide range of biological roles in bacteria. In order to determine the role of H-NS in regulating gene transcription and further find out the biological significance of this protein in EnterohemorrhagicEscherichia coli(EHEC), we conducted transcriptome analysis ofhnsmutant by RNA sequencing. A total of 983 genes were identified to be regulated by H-NS in EHEC. 213 and 770 genes were down-regulated and up-regulated in the deletion mutant ofhns, respectively. Interestingly, 34 of 97 genes on virulence plasmid pO157 were down-regulated by H-NS. Although the deletion mutant ofhnsshowed a decreased survival rate in macrophage compared with the wild type strain, it exhibited the higher ability to colonize mice gut and became more virulent to BALB/c mice. The BALB/c mice infected with the deletion mutant ofhnsshowed a lower survival rate, and a higher bacterial burden in the gut, compared with those infected with wild type strain, especially when the gut microbiota was not disturbed by antibiotic administration. These findings suggest that H-NS plays an important role in virulence of EHEC by interacting with host gut microbiota.