Sun Yi-Cheng, Hinnebusch B Joseph, Darby Creg
Program in Microbial Pathogenesis, Department of Cell and Tissue Biology, University of California, San Francisco, CA 94143, USA.
Proc Natl Acad Sci U S A. 2008 Jun 10;105(23):8097-101. doi: 10.1073/pnas.0803525105. Epub 2008 Jun 3.
Yersinia pestis, the agent of bubonic plague, evolved from the enteric pathogen Yersinia pseudotuberculosis within the past 20,000 years. Because ancestor and descendant both exist, it is possible to infer steps in molecular evolution by direct experimental approaches. The Y. pestis life cycle includes establishment of a biofilm within its vector, the flea. Although Y. pseudotuberculosis makes biofilms in other environments, it fails to do so in the insect. We show that rcsA, a negative regulator of biofilms that is functional in Y. pseudotuberculosis, is a pseudogene in Y. pestis. Replacement of the pseudogene with the functional Y. pseudotuberculosis rcsA allele strongly represses biofilm formation and essentially abolishes flea biofilms. The conversion of rcsA to a pseudogene during Y. pestis evolution, therefore, was a case of negative selection rather than neutral genetic drift.
鼠疫耶尔森菌是腺鼠疫的病原体，在过去2万年里从肠道病原体假结核耶尔森菌进化而来。由于祖先和后代都存在，因此可以通过直接实验方法推断分子进化的步骤。鼠疫耶尔森菌的生命周期包括在其传播媒介跳蚤体内形成生物膜。虽然假结核耶尔森菌在其他环境中能形成生物膜，但在昆虫体内却不能。我们发现，rcsA是一种在假结核耶尔森菌中发挥作用的生物膜负调控因子，在鼠疫耶尔森菌中是一个假基因。用功能性的假结核耶尔森菌rcsA等位基因替换该假基因，可强烈抑制生物膜形成，并基本消除跳蚤体内的生物膜。因此，在鼠疫耶尔森菌进化过程中rcsA转变为假基因是负选择的结果，而非中性遗传漂变。
