Precise excision of the large pathogenicity island, SP17, in Salmonella enterica serovar Typhi
Precise excision of the large pathogenicity island, SP17, in Salmonella enterica serovar Typhi
复制标题
DOI：
10.1128/jb.186.10.3202-3213.2004
复制
发表时间：
2004-05-01
影响因子：
3.2
通讯作者：
Mora, GC
中科院分区：
文献类型：
--
作者：
Bueno, SM;Santiviago, CA;Mora, GC
伤寒沙门氏菌的大致病岛（SPI 7）是一个133，477-bp的DNA片段，侧翼是两个52-bp的与pheU（苯丙氨酰-tRNA）基因重叠的同向重复序列，包含151个潜在的开放阅读框，并且包括参与Vi抗原合成的viaB操纵子。一些临床分离的S.由于精确切除，肠伤寒血清型缺失了整个SPI 7;这些菌株丧失了产生Vi抗原的能力，对噬菌体Vi-II具有抗性，并且更迅速地侵入人上皮细胞系。在临床分离的S.当伤寒沙门氏菌在实验室中生长时，在其新的连接点处留下完整的pheU基因拷贝，并导致相同的三种表型结果。SPI 7是一种不稳定的遗传元件，可能是肠道革兰氏阴性菌之间这种致病岛横向转移途径的中间体。
The large pathogenicity island (SPI7) of Salmonella enterica serovar Typhi is a 133,477-bp segment of DNA flanked by two 52-bp direct repeats overlapping the pheU (phenylalanyl-tRNA) gene, contains 151 potential open reading frames, and includes the viaB operon involved in the synthesis of Vi antigen. Some clinical isolates of S. enterica serovar Typhi are missing the entire SPI7, due to its precise excision; these strains have lost the ability to produce Vi antigen, are resistant to phage Vi-II, and invade a human epithelial cell line more rapidly. Excision of SPI7 occurs spontaneously in a clinical isolate of S. enterica serovar Typhi when it is grown in the laboratory, leaves an intact copy of the pheU gene at its novel join point, and results in the same three phenotypic consequences. SPI7 is an unstable genetic element, probably an intermediate in the pathway of lateral transfer of such pathogenicity islands among enteric gram-negative bacteria.