PoxA、yjeK 和延伸因子 P 协同调节沙门氏菌的毒力和耐药性。
PoxA, yjeK, and elongation factor P coordinately modulate virulence and drug resistance in Salmonella enterica.
机构信息
Department of Molecular Genetics, University of Toronto, Toronto, Ontario, M5S 1A8, Canada.
出版信息
Mol Cell. 2010 Jul 30;39(2):209-21. doi: 10.1016/j.molcel.2010.06.021.
We report an interaction between poxA, encoding a paralog of lysyl tRNA-synthetase, and the closely linked yjeK gene, encoding a putative 2,3-beta-lysine aminomutase, that is critical for virulence and stress resistance in Salmonella enterica. Salmonella poxA and yjeK mutants share extensive phenotypic pleiotropy, including attenuated virulence in mice, an increased ability to respire under nutrient-limiting conditions, hypersusceptibility to a variety of diverse growth inhibitors, and altered expression of multiple proteins, including several encoded on the SPI-1 pathogenicity island. PoxA mediates posttranslational modification of bacterial elongation factor P (EF-P), analogous to the modification of the eukaryotic EF-P homolog, eIF5A, with hypusine. The modification of EF-P is a mechanism of regulation whereby PoxA acts as an aminoacyl-tRNA synthetase that attaches an amino acid to a protein resembling tRNA rather than to a tRNA.
我们报告了 poxA 基因（编码赖氨酸 tRNA 合成酶的一个旁系同源物）与紧邻的 yjeK 基因（编码一个假定的 2,3-β-赖氨酸氨基变位酶）之间的相互作用，这对于沙门氏菌的毒力和应激抗性至关重要。沙门氏菌 poxA 和 yjeK 突变体具有广泛的表型多效性，包括在小鼠中的毒力减弱、在营养限制条件下呼吸能力增强、对多种不同生长抑制剂的敏感性增加以及多种蛋白质的表达改变，包括 SPI-1 致病性岛上编码的几种蛋白质。PoxA 介导细菌延伸因子 P（EF-P）的翻译后修饰，类似于真核 EF-P 同源物 eIF5A 的修饰，用 Hypusine 修饰。EF-P 的修饰是一种调节机制，其中 PoxA 作为氨酰-tRNA 合成酶，将氨基酸连接到类似于 tRNA 的蛋白质上，而不是连接到 tRNA 上。
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