权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Regulation of Bacteroides fragilis capsule expression

脆弱拟杆菌荚膜表达的调节

基本信息

批准号：
6446576
负责人：
CORINNA M KRINOS
金额：
$ 4.62万
依托单位：
BRIGHAM AND WOMEN'S HOSPITAL
依托单位国家：
美国
项目类别：
财政年份：
2002
资助国家：
美国
起止时间：
2002-05-01 至
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/6446576
关键词：
Bacteroides bacterial capsules bacterial genetics bacterial polysaccharides carbohydrate biosynthesis gene expression gene mutation genetic regulation genetic transcription mutant postdoctoral investigator site directed mutagenesis

项目摘要

DESCRIPTION (provided by the applicant): Bacteroides fragilis is the most frequently isolated anaerobic species from human infections such as intra-abdominal abscesses and bacteremia. The capsular polysaccharide complex of this organism has been identified as the primary virulence factor responsible for intra-abdominal abscesses. We identified two conserved genes (upxY and upxz) located upstream of eight distinct polysaccharide biosynthesis regions in a single B. fragilis strain. We hypothesize these products play an important role in the regulation of the capsular polysaccharides of B. fragilis, bestowing upon them a global function for polysaccharide regulation in this species. We have shown that deletion of upcY abrogates the ability of B. fragilis to produce one of its eight polysaccharides, and that this regulation occurs at the transcriptional level. We hypothesize that each tandem pair of genes specifically regulates the polysaccharide biosynthesis locus of which they are a part. An upaY mutant will be created and its phenotype will be analyzed to determine if it has a similar function in the specific regulation of the PS A biosynthesis locus as that of upcY in the regulation of the PS C biosynthesis operon. xylE reporter studies will determine if UpaY acts at the level of transcription to specifically regulate the PS A operon. Site-specific mutagenesis will be performed to determine which amino acids of UpaY are involved in conferring specific regulation of PS A expression. As UpcZ is not homologous to any sequences in the databases we will determine the role and mode of action of UpcZ in the regulation of PS C, by constructing a deletion mutant and performing transcriptional assays.

描述（由申请人提供）：脆弱拟杆菌是最常见的经常从人类感染中分离出厌氧菌，例如腹内脓肿和菌血症。荚膜多糖复合物该生物体已被确定为主要毒力因子导致腹腔内脓肿。我们鉴定出两个保守基因（upxY 和 upxz）位于八种不同多糖生物合成的上游单个脆弱拟杆菌菌株中的区域。我们假设这些产品发挥着 B. 荚膜多糖的调节具有重要作用。 fragilis，赋予它们多糖调节的全局功能在这个物种中。我们已经证明，删除 upcY 会消除 B. fragilis 产生其八种多糖中的一种，并且这种调控发生在转录水平。我们假设每个串联一对基因特异性调控多糖生物合成位点他们是其中的一部分。将创建一个 upaY 突变体，其表型将是分析以确定其在具体法规中是否具有类似功能 PS A 生物合成位点与 upcY 在 PS C 调节中的作用生物合成操纵子。 xylE 记者研究将确定 UpaY 是否在转录水平特异性调节 PSA 操纵子。特定地点将进行诱变以确定 UpaY 的哪些氨基酸参与赋予 PSA 表达的特异性调节。由于 UpcZ 不是与数据库中的任何序列同源，我们将确定其作用和 UpcZ 通过构建缺失来调节 PS C 的作用方式突变体并进行转录测定。