A Salmonella Typhi homologue of bacteriophage muramidases controls typhoid toxin secretion
A Salmonella Typhi homologue of bacteriophage muramidases controls typhoid toxin secretion
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DOI：
10.1038/embor.2012.186
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发表时间：
2013-01-01
期刊：
影响因子：
7.7
通讯作者：
Galan, Jorge E.
中科院分区：
文献类型：
--
作者：
Hodak, Helene;Galan, Jorge E.
与其他沙门氏菌不同，它可以感染广泛的宿主，引起自限性感染，伤寒沙门氏菌是一种专门的人类病原体，导致伤寒，一种危及生命的全身性疾病。伤寒毒素是伤寒沙门氏菌特有的毒力因子，当细菌在哺乳动物细胞内时表达。在这里，我们报告说，N-乙酰-β-D-胞壁酶类似于噬菌体内溶素编码在相同的致病性胰岛内的毒素是伤寒毒素分泌所需的。TtsA的遗传和功能分析揭示了其预测的肽聚糖结合结构域中的独特氨基酸，这些氨基酸对于蛋白质分泌是必需的，并且将该蛋白质与其他同源物区分开来。我们建议，TtsA定义了一个新的蛋白质分泌机制，最近从机器介导的噬菌体释放。
Unlike other Salmonella, which can infect a broad range of hosts causing self-limiting infection, Salmonella Typhi is an exclusively human pathogen that causes typhoid fever, a life-threatening systemic disease. Typhoid toxin is a unique virulence factor of Salmonella Typhi, which is expressed when the bacteria are within mammalian cells. Here, we report that an N-acetyl-beta-D-muramidase similar to phage endolysins encoded within the same pathogenicity islet as the toxin is required for typhoid toxin secretion. Genetic and functional analysis of TtsA revealed unique amino acids at its predicted peptidoglycan-binding domain that are essential for protein secretion and that distinguishes this protein from other homologues. We propose that TtsA defines a new protein secretion mechanism recently evolved from the machine that mediates phage release.