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The cell surface protein Ag43 facilitates phage infection of Escherichia coli in the presence of bile salts and carbohydrates

机译:细胞表面蛋白AG43促进胆汁盐和碳水化合物存在下大肠杆菌的噬菌体感染

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It was found that infection of Escherichia coli by bacteriophage λ is inhibited in the presence of certain bile salts and carbohydrates when cells are in the ’OFF’ state for production of the phase-variable cell surface protein antigen 43 (Ag43). The inhibition of phage growth was found to be due to a significant impairment in the process of phage adsorption. Expression of the gene encoding Ag43 (agn43) from a plasmid or inactivation of the oxyR gene (encoding an activator of genes important for defence against oxidative stress) suppressed this inhibition. A mutation, rpoA341, in the gene encoding the α subunit of RNA polymerase also facilitated phage adsorption in the presence of bile salts and carbohydrates. The rpoA341 mutation promoted efficient production of Ag43 in a genetic background that would otherwise be in the ’OFF’ phase for expression of the agn43 gene. Analysis of a reporter gene fusion demonstrated that the promoter for the agn43 gene was more active in the rpoA341 mutant than in the otherwise isogenic rpoA+ strain. The combined inhibitory action of bile salts and carbohydrates on phage adsorption and the abolition of this inhibition by production of Ag43 was not restricted to λ, as a similar phenomenon was observed for the coliphages P1 and T4.
机译:发现当细胞处于“OFF”状态以产生相变细胞表面蛋白抗原43(AG43)时,在某些胆汁盐和碳水化合物的存在下,在某些胆汁盐和碳水化合物存在下抑制了噬菌体λ的感染。发现噬菌体生长的抑制是由于噬菌体吸附过程中的显着损害。编码Ag43(AgN43)的基因的表达来自氧罗斯基因的质粒或灭活(编码对防御氧化应激的重要的基因激活剂)抑制了这种抑制作用。在编码RNA聚合酶的α亚基的基因中,突变RPOA341还促进了胆汁盐和碳水化合物存在下的噬菌体吸附。 RPOA341突变在遗传背景中促进了Ag43的有效生产,否则在“OFF”期间表达AGN43基因。报告基因融合的分析表明,AgN43基因的启动子在RPOA341突变中更活跃,而不是在其他等原性RPOA +菌株中。胆汁盐和碳水化合物对噬菌体吸附的组合抑制作用和通过产生Ag43的抑制的抑制不限于λ,因为对于Coliphages P1和T4观察到类似的现象。

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