McClelland Michael, Sanderson Kenneth E, Clifton Sandra W, Latreille Phil, Porwollik Steffen, Sabo Aniko, Meyer Rekha, Bieri Tamberlyn, Ozersky Phil, McLellan Michael, Harkins C Richard, Wang Chunyan, Nguyen Christine, Berghoff Amy, Elliott Glendoria, Kohlberg Sara, Strong Cindy, Du Feiyu, Carter Jason, Kremizki Colin, Layman Dan, Leonard Shawn, Sun Hui, Fulton Lucinda, Nash William, Miner Tracie, Minx Patrick, Delehaunty Kim, Fronick Catrina, Magrini Vincent, Nhan Michael, Warren Wesley, Florea Liliana, Spieth John, Wilson Richard K
Sidney Kimmel Cancer Center, 10835 Altman Row, San Diego, California 92121, USA.
Nat Genet. 2004 Dec;36(12):1268-74. doi: 10.1038/ng1470. Epub 2004 Nov 7.
Salmonella enterica serovars often have a broad host range, and some cause both gastrointestinal and systemic disease. But the serovars Paratyphi A and Typhi are restricted to humans and cause only systemic disease. It has been estimated that Typhi arose in the last few thousand years. The sequence and microarray analysis of the Paratyphi A genome indicates that it is similar to the Typhi genome but suggests that it has a more recent evolutionary origin. Both genomes have independently accumulated many pseudogenes among their approximately 4,400 protein coding sequences: 173 in Paratyphi A and approximately 210 in Typhi. The recent convergence of these two similar genomes on a similar phenotype is subtly reflected in their genotypes: only 30 genes are degraded in both serovars. Nevertheless, these 30 genes include three known to be important in gastroenteritis, which does not occur in these serovars, and four for Salmonella-translocated effectors, which are normally secreted into host cells to subvert host functions. Loss of function also occurs by mutation in different genes in the same pathway (e.g., in chemotaxis and in the production of fimbriae).
肠炎沙门氏菌血清型通常具有广泛的宿主范围,有些会引起胃肠道疾病和全身性疾病。但甲型副伤寒沙门氏菌和伤寒沙门氏菌血清型仅感染人类,且只引发全身性疾病。据估计,伤寒沙门氏菌血清型是在过去几千年前出现的。甲型副伤寒沙门氏菌基因组的序列和微阵列分析表明,它与伤寒沙门氏菌基因组相似,但显示其进化起源更近。两个基因组在其大约4400个蛋白质编码序列中都独立积累了许多假基因:甲型副伤寒沙门氏菌中有173个,伤寒沙门氏菌中约有210个。这两个相似基因组最近在相似表型上的趋同微妙地反映在它们的基因型中:两个血清型中只有30个基因发生了降解。然而,这30个基因包括3个已知在肠胃炎中起重要作用的基因(这些血清型不会引发肠胃炎),以及4个沙门氏菌易位效应蛋白基因(这些蛋白通常分泌到宿主细胞中以破坏宿主功能)。功能丧失也通过同一途径中不同基因的突变发生(例如在趋化作用和菌毛产生中)。