INRA, UMR1319 Micalis, Jouy-en-Josas, France.
J Bacteriol. 2013 Jul;195(13):3073-83. doi: 10.1128/JB.00121-13. Epub 2013 May 3.
The Enterococcus faecalis leucine-rich protein ElrA promotes virulence by stimulating bacterial persistence in macrophages and production of the interleukin-6 (IL-6) cytokine. The ElrA protein is encoded within an operon that is poorly expressed under laboratory conditions but induced in vivo. In this study, we identify ef2687 (renamed elrR), which encodes a member of the Rgg (regulator gene for glucosyltransferase) family of putative regulatory proteins. Using quantitative reverse transcription-PCR, translational lacZ fusions, and electrophoretic mobility shift assays, we demonstrate that ElrR positively regulates expression of elrA. These results correlate with the attenuated virulence of the ΔelrR strain in a mouse peritonitis model. Virulence of simple and double elrR and elrA deletion mutants also suggests a remaining ElrR-independent expression of elrA in vivo and additional virulence-related genes controlled by ElrR.
粪肠球菌富含亮氨酸蛋白 ElrA 通过刺激巨噬细胞中的细菌持续存在和白细胞介素-6 (IL-6) 细胞因子的产生来促进毒力。ElrA 蛋白编码在一个操纵子中，该操纵子在实验室条件下表达不佳，但在体内诱导。在这项研究中，我们鉴定了 ef2687（重命名为 elrR），它编码一个假定调节蛋白的 Rgg（葡糖基转移酶调节基因）家族的成员。使用定量逆转录-PCR、翻译 lacZ 融合和电泳迁移率变动分析，我们证明了 ElrR 正向调节 elrA 的表达。这些结果与ΔelrR 菌株在小鼠腹膜炎模型中减弱毒力的情况相关。简单和双 elrR 和 elrA 缺失突变体的毒力也表明体内仍存在 ElrR 不依赖的 elrA 表达，以及由 ElrR 控制的其他与毒力相关的基因。
