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YbeY核糖核酸酶的缺失损害了小肠结肠炎耶尔森氏菌O:3的生长并增强了其毒性质粒基因的表达。

Absence of YbeY RNase compromises the growth and enhances the virulence plasmid gene expression of Yersinia enterocolitica O:3.

作者信息

Leskinen Katarzyna, Varjosalo Markku, Skurnik Mikael

机构信息

Haartman Institute, Department of Bacteriology and Immunology, Research Programs Unit, Immunobiology, University of Helsinki, Finland.

Biocentrum Helsinki, Finland: Finnish Institute of Molecular Medicine, Finland.

出版信息

Microbiology (Reading). 2015 Feb;161(Pt 2):285-299. doi: 10.1099/mic.0.083097-0. Epub 2014 Nov 21.

Abstract

YbeY was recently recognized as an endoribonuclease playing a role in ribosome biosynthesis. In Escherichia coli it functions as a single-strand-specific RNase that processes the 3' end of the 16S rRNA and is crucial for the late-stage 70S ribosome quality control system. Here we report that YbeY is not essential in Yersinia enterocolitica serotype O:3, yet its absence strongly compromised the bacterium. The lack of YbeY resulted in misprocessing of 16S rRNA and a severe decrease of growth rate with complete growth arrest observed at elevated temperatures. Moreover, a ybeY mutation severely disturbed regulation of the Yersinia virulence plasmid (pYV) genes and affected the expression of regulatory small RNA species. Transcription of the pYV genes was upregulated in the ybeY mutant at 22 °C; the same genes were repressed in the wild-type bacterium. Furthermore, ybeY inactivation impaired many virulence-related features, such as resistance to elevated temperature and acid, and hindered utilization of different carbohydrates. In addition, the ybeY mutant strain showed decreased infectivity in a tissue culture infection model, especially at the stage of cell adhesion. Taken together, this study demonstrates the crucial role of YbeY in Y. enterocolitica O:3 physiology and pathogenicity.

摘要

YbeY最近被认为是一种在核糖体生物合成中发挥作用的核糖核酸酶。在大肠杆菌中,它作为一种单链特异性核糖核酸酶发挥作用,加工16S rRNA的3'末端,对后期70S核糖体质量控制系统至关重要。在此我们报告,YbeY在小肠结肠炎耶尔森菌O:3血清型中并非必需,但它的缺失严重损害了该细菌。YbeY的缺失导致16S rRNA加工错误,生长速率严重下降,在高温下观察到完全生长停滞。此外,ybeY突变严重干扰了小肠结肠炎耶尔森菌毒力质粒(pYV)基因的调控,并影响了调控性小RNA种类的表达。在22°C时,pYV基因在ybeY突变体中的转录上调;相同的基因在野生型细菌中受到抑制。此外,ybeY失活损害了许多与毒力相关的特征,如对高温和酸的抗性,并阻碍了不同碳水化合物的利用。此外,ybeY突变体菌株在组织培养感染模型中的感染性降低,尤其是在细胞黏附阶段。综上所述,本研究证明了YbeY在小肠结肠炎耶尔森菌O:3生理和致病性中的关键作用。

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