期刊
MOLECULAR MICROBIOLOGY
卷 58, 期 1, 页码 71-79出版社
WILEY
DOI: 10.1111/j.1365-2958.2005.04806.x
关键词
-
资金
- NIAID NIH HHS [AI43006, AI 17828] Funding Source: Medline
While examining the molecular basis for the lack of actin- based motility for the non- pathogenic spotted fever group ( SFG) R. peacockii, we identified a novel insertion sequence ( IS) element, ISRpe1, disrupting the coding sequence of rickA, demonstrated to induce actin- tail polymerization for the SFG rickett-siae. This rickettsial IS element appears to be active in that complete terminal inverted repeat and recombinase/ transposase open reading frame sequences are present and the transposase is transcriptionally expressed. Phylogenetically, ISRpe1 belongs to a new IS family that is most closely related to those transposable elements of other intracellular bacteria like Wolbachia spp. ISRpe1 was demonstrated to be present in at least 10 locations throughout the R. peacockii genome, including one that disrupted the putative cell surface antigen encoding gene, sca1 considered to be involved in adhesion and virulence of the rickettsiae. Additionally, three IS sites demonstrated rearrangements/ relocations of the R. peacockii genome when compared to those of other SFG rickettsiae. Our findings of the disruptions of rickA and sca1 along with the comparative genomic reassortments associated with ISRpe1 in the non- virulent R. peacockii provides opportunities to uncover molecular mechanisms underlying the pathogenesis and evolution of rickettsiae as well as its potential to be used in rickettsial transposon- based mutagenesis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据