Division of Infectious Diseases, Department of Internal Medicine, University of Texas Medical School at Houston, Texas 77030, USA.
J Infect Dis. 2011 Apr 15;203(8):1147-54. doi: 10.1093/infdis/jiq160.
General stress proteins, Gls24 and GlsB, were previously shown to be involved in bile salts resistance of Enterococcus faecalis and in virulence. Here, we identified 2 gene clusters in Enterococcus faecium each encoding a homolog of Gls24 (Gls33 and Gls20; designated on the basis of their predicted sizes) and of GlsB (GlsB and GlsB1). The sequences of the gls33 and gls20 gene clusters from available genomes indicate distinct lineages, with those of hospital-associated CC17 isolates differing from non-CC17 by ∼7% and ∼3.5%, respectively. Deletion of an individual locus did not have a significant effect on virulence in a mouse peritonitis model, whereas a double-deletion mutant was highly attenuated (P<.004) versus wild-type. However, mutants lacking either gls33-glsB, gls20-glsB1, or both all exhibited increased sensitivity to bile salts. These results suggest that gls-encoded loci may be important for adaptation to the intestinal environment, in addition to being important for virulence functions.
先前的研究表明，一般应激蛋白 Gls24 和 GlsB 参与粪肠球菌对胆盐的抗性和毒力。在这里，我们在屎肠球菌中鉴定了 2 个基因簇，每个基因簇都编码 Gls24（Gls33 和 Gls20；根据其预测大小命名）和 GlsB（GlsB 和 GlsB1）的同源物。来自可用基因组的 gls33 和 gls20 基因簇序列表明存在不同的谱系，与医院相关的 CC17 分离株之间的差异分别约为 7%和 3.5%。在小鼠腹膜炎模型中，单独缺失一个基因座对毒力没有显著影响，而双缺失突变体的毒力显著减弱（P<.004）。然而，缺失 gls33-glsB、gls20-glsB1 或两者的突变体均表现出对胆盐的敏感性增加。这些结果表明，gls 编码的基因座除了对毒力功能很重要外，可能对适应肠道环境也很重要。
