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

Lina Laskos, Joseph P. Dillard, H. Steven Seifert, Janet A.M. Fyfe, John K. Davies*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

Abstract

The σ54 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.

Original languageEnglish (US)
Pages (from-to)95-102
Number of pages8
JournalGene
Volume208
Issue number1
DOIs
StatePublished - Feb 16 1998

Keywords

  • Gonococcus
  • Pili
  • RLS
  • RpoN

ASJC Scopus subject areas

  • Genetics

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