Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype.

Chromosomal instability in enterohaemorrhagic Escherichia coli O157:H7: impact on adherence, tellurite resistance and colony phenotype.
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DOI:
10.1111/j.1365-2958.2010.07499.x
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发表时间:
2011-02
影响因子:
3.6
通讯作者:
Mellmann A
Mellmann A
中科院分区:
生物学2区
文献类型:
--
作者:
Bielaszewska M;Middendorf B;Tarr PI;Zhang W;Prager R;Aldick T;Dobrindt U;Karch H;Mellmann A

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耐亚碲酸盐肠出血性大肠杆菌(EHEC)O 157:H7是一种全球性病原体。在菌株EDL 933中,Tel抗性(TelR)由O岛(OI)43和48中的重复ter簇编码,所述O岛43和48也含有编码粘附素和铁载体受体Iha的iha。我们鉴定了5株肠出血性大肠杆菌O 157:H7菌株,它们分别分化为具有高和低Tel最小抑菌浓度(MIC)的大(L)菌落和小(S)菌落。S菌落(Tel-MIC ≤ 4 µg ml−1)通过IS元件之间的同源重组以及丢失的ter和iha,在TelR OI内维持大的内部缺失。此外,完全切除的岛屿发生侧翼的直接重复序列之间的位点特异性重组。在培养的细胞中,OI 43和OI 48的完全切除分别发生在1.81 × 10−3和1.97 × 10−4个细胞中; OI 48的内部缺失更常见(9.7 × 10−1个细胞)。在促进iha转录的铁限制下,iha阴性衍生物与人肠上皮细胞的粘附性较差,生长速度也比iha阳性衍生物慢。利用IHA缺失和互补突变体的实验确定IHA为负责这些表型差异的主要因素。影响TelR OIs的自发缺失有助于EHEC O 157基因组的可塑性,并可能损害毒力和/或适应性。
Tellurite (Tel) resistant enterohaemorrhagic Escherichia coli (EHEC) O157:H7 is a global pathogen. In strain EDL933 Tel resistance (TelR) is encoded by duplicate ter cluster in O islands (OI) 43 and 48, which also harbour iha, encoding the adhesin and siderophore receptor Iha. We identified five EHEC O157:H7 strains that differentiate into large (L) colonies and small (S) colonies with high and low Tel minimal inhibitory concentrations (MICs) respectively. S colonies (Tel-MICs ≤ 4 µg ml−1) sustained large internal deletions within the TelR OIs via homologous recombination between IS elements and lost ter and iha. Moreover, complete excision of the islands occurred by site-specific recombination between flanking direct repeats. Complete excision of OI 43 and OI 48 occurred in 1.81 × 10−3 and 1.97 × 10−4 cells in culture, respectively; internal deletion of OI 48 was more frequent (9.7 × 10−1 cells). Under iron limitation that promotes iha transcription, iha-negative derivatives adhered less well to human intestinal epithelial cells and grew slower than did their iha-positive counterparts. Experiments utilizing iha deletion and complementation mutants identified Iha as the major factor responsible for these phenotypic differences. Spontaneous deletions affecting TelR OIs contribute to EHEC O157 genome plasticity and might impair virulence and/or fitness.
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