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首页> 外文期刊>Molecular Microbiology >Mutation of praR in Rhizobium leguminosarum enhances root biofilms, improving nodulation competitiveness by increased expression of attachment proteins
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Mutation of praR in Rhizobium leguminosarum enhances root biofilms, improving nodulation competitiveness by increased expression of attachment proteins

机译：豆根瘤菌中praR的突变增强了根部生物膜，通过增加附着蛋白的表达提高了结瘤竞争能力

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In Rhizobium leguminosarum bv. viciae, quorum-sensing is regulated by CinR, which induces the cinIS operon. CinI synthesizes an AHL, whereas CinS inactivates PraR, a repressor. Mutation of praR enhanced biofilms in vitro. We developed a light (lux)-dependent assay of rhizobial attachment to roots and demonstrated that mutation of praR increased biofilms on pea roots. The praR mutant out-competed wild-type for infection of pea nodules in mixed inoculations. Analysis of gene expression by microarrays and promoter fusions revealed that PraR represses its own transcription and mutation of praR increased expression of several genes including those encoding secreted proteins (the adhesins RapA2, RapB and RapC, two cadherins and the glycanase PlyB), the polysaccharide regulator RosR, and another protein similar to PraR. PraR bound to the promoters of several of these genes indicating direct repression. Mutations in rapA2, rapB, rapC, plyB, the cadherins or rosR did not affect the enhanced root attachment or nodule competitiveness of the praR mutant. However combinations of mutations in rapA, rapB and rapC abolished the enhanced attachment and nodule competitiveness. We conclude that relief of PraR-mediated repression determines a lifestyle switch allowing the expression of genes that are important for biofilm formation on roots and the subsequent initiation of infection of legume roots.
机译：在豆科根瘤菌中。蚕豆，群体感应受CinR调节，CinR诱导cinIS操纵子。 CinI合成AHL，而CinS灭活阻遏物PraR。 praR突变体外增强了生物膜。我们开发了根茎与根的附着的光（勒克斯）依赖性测定法，并证明praR突变增加了豌豆根上的生物膜。 praR突变体在混合接种中对豌豆结节的感染胜过野生型。通过微阵列和启动子融合蛋白对基因表达进行的分析表明，PraR抑制了自身的转录，而praR突变使包括编码分泌蛋白（粘附素RapA2，RapB和RapC，两个钙黏着蛋白和聚糖酶PlyB）在内的几种基因的表达增加，多糖调节剂RosR和另一种类似于PraR的蛋白质。 PraR结合到这些基因中的几个基因的启动子上，指示直接阻遏。 rapA2，rapB，rapC，plyB，钙粘着蛋白或rosR中的突变不会影响praR突变体的根系附着力或根瘤竞争力。然而，rapA，rapB和rapC中突变的组合消除了增强的附着力和结节竞争力。我们得出的结论是，PraR介导的抑制作用的缓解决定了生活方式的转变，允许表达对根部生物膜形成以及随后的豆科植物根部感染至关重要的基因表达。

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