The pathogenic neisseriae contain an inactive rpoN gene and do not utilize the pilE σ54 promoter

被引:33
作者
Laskos, L
Dillard, JP
Seifert, HS
Fyfe, JAM
Davies, JK [1 ]
机构
[1] Monash Univ, Dept Microbiol, Clayton, Vic 3168, Australia
[2] Northwestern Univ, Dept Microbiol Immunol, Chicago, IL 60611 USA
关键词
RpoN; RLS; Pili; gonococcus;
D O I
10.1016/S0378-1119(97)00664-1
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The sigma(54) promoter (P3) upstream of the pilE gene in Neisseria gonorrhoeae was shown to be non-functional by transcriptional analysis of a PpilE::lacZ fusion containing only P3. A region on the chromosome of N. gonorrhoeae strain MS11-A was identified that potentially encodes a protein with a significant similarity to the Escherichia coli RpoN protein. However, this region (designated RLS for rpoN-like sequence) does not contain a single open reading frame (ORF) capable of encoding a functional RpoN protein. It appears that RLS may have arisen from an ancestral rpoN homologue that underwent a deletion removing the sequence encoding the essential helix-turn-helix (HTH) motif, and changing the subsequent reading frame. An RLS has been identified in several strains of N. gonorrhoeae and N. meningitidis. A 90-kDa gonococcal protein has previously been shown to react with a monoclonal antibody raised against the RpoN from Salmonella typhimurium. However, mutagenesis and Western blot analysis confirmed that the gene encoding this protein is not contained within RLS. (C) 1998 Elsevier Science B.V.
引用
收藏
页码:95 / 102
页数:8
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