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首页> 外文期刊>Applied Microbiology >Phage-Encoded Colanic Acid-Degrading Enzyme Permits Lytic Phage Infection of a Capsule-Forming Resistant Mutant Escherichia coli Strain
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Phage-Encoded Colanic Acid-Degrading Enzyme Permits Lytic Phage Infection of a Capsule-Forming Resistant Mutant Escherichia coli Strain

机译：噬菌体编码的Colanic降解酶允许溶菌噬菌体感染的胶囊形成抗性突变大肠杆菌菌株。

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In this study, we isolated a bacteriophage T7-resistant mutant strain of Escherichia coli (named S3) and then proceeded to characterize it. The mutant bacterial colonies appeared to be mucoid. Microarray analysis revealed that genes related to colanic acid production were upregulated in the mutant. Increases in colanic acid production by the mutant bacteria were observed when l-fucose was measured biochemically, and protective capsule formation was observed under an electron microscope. We found a point mutation in the lon gene promoter in S3, the mutant bacterium. Overproduction of colanic acid was observed in some phage-resistant mutant bacteria after infection with other bacteriophages, T4 and lambda. Colanic acid overproduction was also observed in clinical isolates of E. coli upon phage infection. The overproduction of colanic acid resulted in the inhibition of bacteriophage adsorption to the host. Biofilm formation initially decreased shortly after infection but eventually increased after 48 h of incubation due to the emergence of the mutant bacteria. Bacteriophage PBECO4 was shown to infect the colanic acid-overproducing mutant strains of E. coli . We confirmed that the gene product of open reading frame 547 (ORF547) of PBECO4 harbored colanic acid-degrading enzymatic (CAE) activity. Treatment of the T7-resistant bacteria with both T7 and PBECO4 or its purified enzyme (CAE) led to successful T7 infection. Biofilm formation decreased with the mixed infection, too. This procedure, using a phage cocktail different from those exploiting solely receptor differences, represents a novel strategy for overcoming phage resistance in mutant bacteria.
机译：在这项研究中，我们分离了大肠杆菌的噬菌体抗T7突变株（命名为S3），然后对其进行了表征。突变的细菌菌落似乎是粘液样的。基因芯片分析表明，与可乐酸生产有关的基因在突变体中被上调。当用生化法测定l-岩藻糖时，观察到突变细菌产生的可乐酸产量增加，并且在电子显微镜下观察到保护性胶囊的形成。我们在突变细菌S3的lon基因启动子中发现了点突变。在感染了其他噬菌体T4和λ后，在某些对噬菌体具有抗性的突变细菌中发现了可乐酸的过量生产。噬菌体感染后在大肠杆菌的临床分离株中也发现了钴酸的过量生产。过多的可乐酸导致抑制噬菌体吸附到宿主。感染后不久，生物膜的形成开始减少，但由于突变细菌的出现，在孵育48小时后最终增加。噬菌体PBECO4显示出感染大肠杆菌中产生可乐酸的突变株。我们确认，PBECO4的开放阅读框547（ORF547）的基因产物具有可乐酸降解酶（CAE）活性。用T7和PBECO4或其纯化的酶（CAE）处理对T7耐药的细菌导致成功的T7感染。生物膜的形成也因混合感染而减少。该程序使用不同于仅利用受体差异的噬菌体混合物的噬菌体混合物，代表了克服突变细菌中噬菌体抗性的新策略。

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