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首页> 外文期刊>Applied Microbiology >Identification and Characterization of Spontaneous Deletions within the Sp11-Sp12 Prophage Region of Escherichia coli O157:H7 Sakai
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Identification and Characterization of Spontaneous Deletions within the Sp11-Sp12 Prophage Region of Escherichia coli O157:H7 Sakai

机译：鉴定和鉴定O157：H7 Sakai大肠菌Sp11-Sp12噬菌体区域内的自发缺失

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Prophages make up 12% of the enterohemorrhagic Escherichia coli genome and play prominent roles in the evolution and virulence of this food-borne pathogen. Acquisition and loss of and rearrangements within prophage regions are the primary causes of differences in pulsed-field gel electrophoresis (PFGE) patterns among strains of E. coli O157:H7. Sp11 and Sp12 are two tandemly integrated and putatively defective prophages carried by E. coli O157:H7 strain Sakai. In this study, we identified 3 classes of deletions that occur within the Sp11-Sp12 region, at a frequency of ca. 7.74 × 10~(?4). One deletion resulted in a precise excision of Sp11, and the other two spanned the junction of Sp11 and Sp12. All deletions resulted in shifts in the XbaI fragment pattern observed by PFGE. We sequenced the inducible prophage pool of Sakai but did not identify any mature phage particles corresponding to either Sp11 or Sp12. Deletions containing pchB and psrC , which are Sp11-carried genes encoding proteins known or suspected to regulate type III secretion, did not affect the secretion levels of the EspA or EspB effector. Alignment of the Sp11-Sp12 DNA sequence with its corresponding regions in other E. coli O157:H7 and O55:H7 strains suggested that homologous recombination rather than integrase-mediated excision is the mechanism behind these deletions. Therefore, this study provides a mechanism behind the previously observed genetic instability of this genomic region of E. coli O157:H7.
机译：噬菌体占肠出血性大肠杆菌基因组的12％，并在这种食源性病原体的进化和毒力中发挥重要作用。噬菌体区域内的采集，丢失和重排是大肠杆菌O157：H7菌株之间脉冲场凝胶电泳（PFGE）模式差异的主要原因。 Sp11和Sp12是大肠杆菌O157：H7株Sakai携带的两个串联整合且推定有缺陷的原噬菌体。在这项研究中，我们确定了Sp11-Sp12区域内发生频率为ca的3类缺失。 7.74×10〜（？4）。一个删除导致Sp11的精确切除，另外两个删除了Sp11和Sp12的交界处。所有缺失均导致PFGE观察到的XbaI片段模式发生变化。我们对酒井的诱导型噬菌体池进行了测序，但未发现与Sp11或Sp12对应的任何成熟噬菌体颗粒。含有pchB和psrC的缺失是Sp11携带的基因，其编码已知或怀疑可调节III型分泌的蛋白质，但不会影响EspA或EspB效应子的分泌水平。 Sp11-Sp12 DNA序列与其他大肠杆菌O157：H7和O55：H7菌株中相应区域的比对表明，同源重组而不是整合酶介导的切除是这些缺失的机制。因此，这项研究为大肠杆菌O157：H7这个基因组区域先前观察到的遗传不稳定性提供了一种机制。

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