Ogura Yoshitoshi, Ooka Tadasuke, Terajima Jun, Nougayrède Jean-Philippe, Kurokawa Ken, Tashiro Kousuke, Tobe Toru, Nakayama Keisuke, Kuhara Satoru, Oswald Eric, Watanabe Haruo, Hayashi Tetsuya
Division of Bioenvironmental Science, Frontier Science Research Center, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki, Japan.
Genome Biol. 2007;8(7):R138. doi: 10.1186/gb-2007-8-7-r138.
Enterohemorrhagic Escherichia coli (EHEC) O157 causes severe food-borne illness in humans. The chromosome of O157 consists of 4.1 Mb backbone sequences shared by benign E. coli K-12, and 1.4 Mb O157-specific sequences encoding many virulence determinants, such as Shiga toxin genes (stx genes) and the locus of enterocyte effacement (LEE). Non-O157 EHECs belonging to distinct clonal lineages from O157 also cause similar illness in humans. According to the 'parallel' evolution model, they have independently acquired the major virulence determinants, the stx genes and LEE. However, the genomic differences between O157 and non-O157 EHECs have not yet been systematically analyzed.
Using microarray and whole genome PCR scanning analyses, we performed a whole genome comparison of 20 EHEC strains of O26, O111, and O103 serotypes with O157. In non-O157 EHEC strains, although genome sizes were similar with or rather larger than O157 and the backbone regions were well conserved, O157-specific regions were very poorly conserved. Around only 20% of the O157-specific genes were fully conserved in each non-O157 serotype. However, the non-O157 EHECs contained a significant number of virulence genes that are found on prophages and plasmids in O157, and also multiple prophages similar to, but significantly divergent from, those in O157.
Although O157 and non-O157 EHECs have independently acquired a huge amount of serotype- or strain-specific genes by lateral gene transfer, they share an unexpectedly large number of virulence genes. Independent infections of similar but distinct bacteriophages carrying these virulence determinants are deeply involved in the evolution of O157 and non-O157 EHECs.
肠出血性大肠杆菌（EHEC）O157可导致人类严重的食源性疾病。O157的染色体由与良性大肠杆菌K-12共享的4.1 Mb主干序列，以及1.4 Mb的O157特异性序列组成，这些特异性序列编码许多毒力决定因素，如志贺毒素基因（stx基因）和肠细胞脱落位点（LEE）。与O157属于不同克隆谱系的非O157 EHEC也可导致人类患类似疾病。根据“平行”进化模型，它们独立获得了主要毒力决定因素，即stx基因和LEE。然而，O157和非O157 EHEC之间的基因组差异尚未得到系统分析。
我们使用微阵列和全基因组PCR扫描分析，对20株O26、O111和O103血清型的EHEC菌株与O157进行了全基因组比较。在非O157 EHEC菌株中，尽管基因组大小与O157相似或略大于O157，且主干区域保守性良好，但O157特异性区域的保守性非常差。在每个非O157血清型中，仅约20%的O157特异性基因完全保守。然而，非O157 EHEC含有大量在O157的原噬菌体和质粒上发现的毒力基因，以及多个与O157中的原噬菌体相似但明显不同的原噬菌体。
尽管O157和非O157 EHEC通过横向基因转移独立获得了大量血清型或菌株特异性基因，但它们共享数量惊人的毒力基因。携带这些毒力决定因素的相似但不同的噬菌体的独立感染在O157和非O157 EHEC的进化中起了重要作用。
