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首页> 外文期刊>Microbial Pathogenesis >Genetic dissection of the Streptococcus pyogenes M1 protein: regions involved in fibronectin binding and intracellular invasion
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Genetic dissection of the Streptococcus pyogenes M1 protein: regions involved in fibronectin binding and intracellular invasion

机译：化脓性链球菌M1蛋白的遗传解剖：涉及纤连蛋白结合和细胞内侵袭的区域

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摘要

Entry of serotype M1 Streptococcus pyogenes into host cells depends on binding of the host glycoprotein fibronectin (Fn) by the bacterial M1 protein. The present study was undertaken to localize the Fn binding region in M1 and assess other potential functions of M1. A set of recombinant M1 protein fragments were assayed for their capacities to bind Fn and inhibit ingestion of streptococci by epithelial cells. M1 protein, M6 protein and internally-deleted derivatives of M1 were expressed on the surface of Lactococcus lactis. Lactococci that expressed M1 or M6 protein bound Fn and were efficiently taken up by epithelial cells. Deletion of both the N-terminal A and B repeats regions of M1 abrogated Fn binding and intracellular invasion. Deletion of either the A domain (M1 DeltaA) or B repeats (M1 DeltaB) significantly reduced, but did not completely eliminate, Fn binding indicating that M1 protein may possess two independent Fn binding sites. Fn binding by the M1 DeltaA or M1 DeltaB proteins was insufficient for efficient invasion, however, suggesting that M protein binding alters the structure of Fn that, in turn, affects the interaction between Fn and epithelial cells. Although expression of M1, M6 or M1 AB proteins led to aggregation of lactococcal cells, aggregation did not significantly contribute to invasion efficiency.
机译：血清型M1化脓性链球菌进入宿主细胞取决于细菌M1蛋白与宿主糖蛋白纤连蛋白（Fn）的结合。进行本研究以定位M1中的Fn结合区并评估M1的其他潜在功能。测定了一组重组M1蛋白片段结合Fn并抑制上皮细胞摄取链球菌的能力。 M1蛋白，M6蛋白和M1的内部缺失衍生物在乳酸乳球菌的表面表达。表达M1或M6蛋白的乳球菌结合Fn，并被上皮细胞有效吸收。 N末端A和B的缺失重复了M1的区域，从而消除了Fn结合和细胞内侵袭。 A结构域（M1 DeltaA）或B重复序列（M1 DeltaB）的缺失显着减少，但并未完全消除Fn结合，表明M1蛋白可能具有两个独立的Fn结合位点。但是，Mn DeltaA或M1 DeltaB蛋白与Fn的结合不足以有效入侵，这表明M蛋白的结合会改变Fn的结构，进而影响Fn与上皮细胞之间的相互作用。尽管M1，M6或M1 AB蛋白的表达导致了乳球菌细胞的聚集，但是聚集并没有显着促进入侵效率。

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