首页> 美国卫生研究院文献>Journal of Bacteriology >Flavobacterium johnsoniae GldK GldL GldM and SprA Are Required for Secretion of the Cell Surface Gliding Motility Adhesins SprB and RemA
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Flavobacterium johnsoniae GldK GldL GldM and SprA Are Required for Secretion of the Cell Surface Gliding Motility Adhesins SprB and RemA

机译:约翰逊黄杆菌GldKGldLGldM和SprA是分泌细胞表面滑行运动粘附素SprB和RemA所必需的

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摘要

Flavobacterium johnsoniae cells move rapidly over surfaces by gliding motility. Gliding results from the movement of adhesins such as SprB and RemA along the cell surface. These adhesins are delivered to the cell surface by a Bacteroidetes-specific secretion system referred to as the type IX secretion system (T9SS). GldN, SprE, SprF, and SprT are involved in secretion by this system. Here we demonstrate that GldK, GldL, GldM, and SprA are each also involved in secretion. Nonpolar deletions of gldK, gldL, or gldM resulted in the absence of gliding motility and in T9SS defects. The mutant cells produced SprB and RemA proteins but failed to secrete them to the cell surface. The mutants were resistant to phages that use SprB or RemA as a receptor, and they failed to attach to glass, presumably because of the absence of cell surface adhesins. Deletion of sprA resulted in similar but slightly less dramatic phenotypes. sprA mutant cells failed to secrete SprB and RemA, but cells remained susceptible to some phages and retained some limited ability to glide. The phenotype of the sprA mutant was similar to those previously described for sprE and sprT mutants. SprA, SprE, and SprT are needed for secretion of SprB and RemA but may not be needed for secretion of other proteins targeted to the T9SS. Genetic and molecular experiments demonstrate that gldK, gldL, gldM, and gldN form an operon and suggest that the proteins encoded by these genes may interact to form part of the F. johnsoniae T9SS.
机译:约翰逊黄杆菌细胞通过滑动运动在表面上快速移动。滑动是由于粘附蛋白(例如SprB和RemA)沿细胞表面移动而引起的。这些粘附素通过称为IX型分泌系统(T9SS)的拟杆菌特有的分泌系统传递至细胞表面。 GldN,SprE,SprF和SprT参与此系统的分泌。在这里,我们证明GldK,GldL,GldM和SprA也都参与分泌。 gldK,gldL或gldM的非极性缺失导致滑行运动的缺失和T9SS缺陷。突变细胞产生SprB和RemA蛋白,但无法将它们分泌到细胞表面。突变体对使用SprB或RemA作为受体的噬菌体具有抗性,并且它们可能无法附着在玻璃上,这可能是因为缺少细胞表面粘附素。删除sprA导致相似但略少的戏剧性表型。 sprA突变细胞无法分泌SprB和RemA,但细胞仍然易受某些噬菌体的侵袭,并保持有限的滑动能力。 sprA突变体的表型与先前针对sprE和sprT突变体所述的表型相似。 SprA,SprE和SprT是分泌SprB和RemA所必需的,而分泌针对T9SS的其他蛋白质则可能不是必需的。遗传和分子实验证明gldK,gldL,gldM和gldN形成操纵子,并暗示这些基因编码的蛋白质可能相互作用形成约翰逊F.T9SS的一部分。

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