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首页> 外文期刊>Scientific reports. >Transcription Elongation Factor GreA Plays a Key Role in Cellular Invasion and Virulence of Francisella tularensis subsp. novicida
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Transcription Elongation Factor GreA Plays a Key Role in Cellular Invasion and Virulence of Francisella tularensis subsp. novicida

机译：转录延伸因子GreA在土拉弗朗西斯菌亚种的细胞侵袭和毒力中起关键作用。诺维达

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摘要

Francisella tularensis is a facultative intracellular Gram-negative bacterium that causes the zoonotic disease tularemia. We identified the transcription elongation factor GreA as a virulence factor in our previous study, but its role was not defined. Here, we investigate the effects of the inactivation of the greA gene, generating a greA mutant of F. tularensis subsp. novicida. Inactivation of greA impaired the bacterial invasion into and growth within host cells, and subsequently virulence in mouse infection model. A transcriptomic analysis (RNA-Seq) showed that the loss of GreA caused the differential expression of 196 bacterial genes, 77 of which were identified as virulence factors in previous studies. To confirm that GreA regulates the expression of virulence factors involved in cell invasion by Francisella, FTN_1186 (pepO) and FTN_1551 (ampD) gene mutants were generated. The ampD deletion mutant showed reduced invasiveness into host cells. These results strongly suggest that GreA plays an important role in the pathogenesis of Francisella by affecting the expression of virulence genes and provide new insights into the complex regulation of Francisella infection.
机译：图拉弗朗西斯菌是一种兼性的细胞内革兰氏阴性细菌，可引起人畜共患疾病图拉血病。我们在先前的研究中将转录延伸因子GreA确定为一种毒力因子，但其作用尚未定义。在这里，我们调查了greA基因失活的影响，产生了F. tularensis亚种的greA突变体。诺维达greA的失活会破坏细菌侵入宿主细胞并在宿主细胞内生长，并随后破坏小鼠感染模型中的毒力。转录组分析（RNA-Seq）显示，GreA的缺失导致196个细菌基因的差异表达，其中有77个细菌基因在先前的研究中被鉴定为毒力因子。为了确认GreA调节了弗朗西斯菌侵袭细胞所涉及的毒力因子的表达，生成了FTN_1186（pepO）和FTN_1551（ampD）基因突变体。 ampD缺失突变体显示出对宿主细胞的侵袭力降低。这些结果强烈表明，GreA通过影响毒力基因的表达在弗朗西斯菌的发病机理中发挥重要作用，并为弗朗西斯菌感染的复杂调控提供了新的见解。

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