Identification and molecular characterization of an N-acetylmuramyl-L-alanine amidase Sle1 involved in cell separation of Staphylococcus aureus
Identification and molecular characterization of an N-acetylmuramyl-L-alanine amidase Sle1 involved in cell separation of Staphylococcus aureus
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DOI：
10.1111/j.1365-2958.2005.04881.x
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发表时间：
2005-11-01
影响因子：
3.6
通讯作者：
Sugai, M
中科院分区：
文献类型：
--
作者：
Kajimura, J;Fujiwara, T;Sugai, M
我们从金黄色葡萄球菌atl无效突变体中纯化了参与细胞分离的肽聚糖水解酶，并鉴定了其基因。基因产物的表征显示了32 kDa的N-乙酰胞壁酰-L-丙氨酸酰胺酶，我们将其命名为Sle 1。肽聚糖酶的分析表明，Sle 1优先切割N-乙酰胞壁酰-L-Ala键的二聚体的交叉桥，连接两个murein链的肽聚糖。sle 1的插入突变损害细胞分离并诱导S.金黄色葡萄球菌形成簇，表明Sle 1参与了S.金黄色。使用急性感染小鼠模型，Sle 1突变体揭示了发病机制的显著降低。Atl是S.金黄色葡萄球菌，其已经涉及S.金黄色。atl/sle 1双突变体的产生表明突变体细胞分离严重受损，表明S.金黄色葡萄球菌使用两种肽聚糖水解酶At 1和Sle 1进行细胞分离。与Atl不同，Sle 1不直接参与S的自溶。金黄色。
We purified a peptidoglycan hydrolase involved in cell separation from a Staphylococcus aureus atl null mutant and identified its gene. Characterization of the gene product shows a 32 kDa N-acetylmuramyl-L-alanine amidase that we designated Sle1. Analysis of peptidoglycan digests showed Sle1 preferentially cleaved N-acetylmuramyl-L-Ala bonds in dimeric cross-bridges that interlink the two murein strands in the peptidoglycan. An insertion mutation of sle1 impaired cell separation and induced S. aureus to form clusters suggesting Sle1 is involved in cell separation of S. aureus. The Sle1 mutant revealed a significant decrease in pathogenesis using an acute infection mouse model. Atl is the major autolysin of S. aureus, which has been implicated in cell separation of S. aureus. Generation of an atl/sle1 double mutant revealed that the mutant cell separation was heavily impaired suggesting that S. aureus uses two peptidoglycan hydrolases, Atl and Sle1, for cell separation. Unlike Atl, Sle1 is not directly involved in autolysis of S. aureus.