大肠杆菌噬菌体诱导的染色体岛有助于辅助噬菌体复制并抑制LEE致病性岛

Kat Pick, Lauren Stadel, Tracy L Raivio
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引用次数: 0

摘要

在这项研究中,我们鉴定和表征了在共生大肠杆菌MP1中发现的一种新的噬菌体诱导染色体岛。这个新元件ecimp1是由温带辅助噬菌体vB_EcoP_Kapi1诱导和动员的。ecimp1有助于对其辅助噬菌体的重复感染免疫,影响细菌竞争结果。通过对EcCIMP1的遗传分析,我们发现了一种可能的转录抑制因子,它可以沉默啮齿类鼠柠檬酸杆菌毒力基因的表达。我们还发现了一种由EcCIMP1编码的推定切除酶,矛盾的是,它不促进EcCIMP1的切除,而是支持辅助噬菌体的切除。另一种假定的由一种假定的整合共轭元件编码的切除酶也可以支持vB_EcoP_Kapi1的切除,这表明来自同一细胞内多个类别的可移动遗传元件的切除酶之间存在串扰。尽管在系统发育上与其他表征的噬菌体诱导染色体岛存在距离,但EcCIMP1和EcCIMP1样元件在世界各地的大肠杆菌致病性和共生分离株中普遍存在,这强调了表征这些丰富的遗传元件的重要性。
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Escherichia coli phage-inducible chromosomal island aids helper phage replication and represses the LEE pathogenicity island
In this study, we identify and characterize a novel phage-inducible chromosomal island found in commensal Escherichia coli MP1. This novel element, EcCIMP1, is induced and mobilized by the temperate helper phage vB_EcoP_Kapi1. EcCIMP1 contributes to superinfection immunity against its helper phage, impacting bacterial competition outcomes. Genetic analysis of EcCIMP1 led us to uncover a putative transcriptional repressor, which silences virulence gene expression in the murine pathogen Citrobacter rodentium. We also found a putative excisionase encoded by EcCIMP1 which paradoxically does not promote excision of EcCIMP1, but rather supports excision of the helper phage. Another putative excisionase encoded by a presumed integrative conjugative element can also support excision of vB_EcoP_Kapi1, demonstrating crosstalk between excisionases from multiple classes of mobile genetic elements within the same cell. Although phylogenetically distant from other characterized phage-inducible chromosomal islands, EcCIMP1 and EcCIMP1-like elements are prevalent in both pathogenic and commensal isolates of Escherchia coli from around the world, underscoring the importance of characterizing these abundant genetic elements.
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