Detection and mutation of a luxS-encoded autoinducer in Proteus mirabilis The GenBank accession number for the sequence reported in this paper is AY044337.

Abstract

Quorum sensing regulates the expression of virulence factors in a wide variety of pathogenic bacteria. This study has shown that Proteus mirabilis harbours a homologue of luxS, a gene required for the synthesis of the quorum sensing autoinducer 2 (AI-2). AI-2 activity is expressed during and is correlated with the initiation of swarming migration on agar surfaces. The P. mirabilis luxS locus was cloned and a LuxS N strain constructed by allelic-exchange mutagenesis. While lacking AI-2 activity, a null mutation in luxS, however, did not affect swimming or swarming motility, swarmer cell differentiation, or virulence in a mouse model of ascending urinary tract infection.

Effects of Quorum Sensing on flaA Transcription and Autoagglutination in Campylobacter jejuni

“…The flaA gene is the major gene for flagellin production and motility (13,23,32). The flaA gene carries consensus promoter sequences for σ 28 and flaB has promoter sequences for σ 54 (13,14). Differential expression of two different flagellin genes enables bacteria to respond to different environmental conditions (2,3).…”

“…At this time we cannot explain such a reduction as being caused directly or indirectly by the action of AI-2. We hypothesized that quorum sensing might control flaA transcription via σ 28 and/or anti-σ 28 factors, coordination of which is known to be related to the late stage of flagellar synthesis such as the flagellar motor and chemotaxis in S. enterica serovar Typhimurium (6). Although anti-σ 28 factor was assumed to be absent in H. pylori and C. jejuni (25), recent studies on H. pylori proposed its presence in C. jejuni (7).…”

Potential Emergence of Multi-quorum Sensing Inhibitor Resistant (MQSIR) Bacteria

“…are also known to possess multiple systems and signals ( Table 2). The QS signals modulating these QSS range from unsubstituted-to substituted-HSLs, as well as peptides (DKPs), quinolones, hormones [69,[94][95][96][97][98][99][100][101][102][103][104][105]. In Yersinia, luxI/R homologues are majorly regulated by substituted AHLs [106][107][108].…”

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

“…The genomes of many bacterial species, notably Escherichia coli, Salmonella enterica serovar Typhimurium, Shigella flexneri, Proteus mirabilis, Vibrio cholerae, Vibrio vulnificus, Campylobacter jejuni, Porphyromonas gingivalis, Bacillus subtilis, Streptococcus pyogenes, Streptococcus mutans, Clostridium perfringens and Clostridium difficile, include luxS homologues. In several of these, luxS-related AI-2 signals are involved in bacterial characteristics such as biofilm formation (Balestrino et al, 2005;Blehert et al, 2003;Fong et al, 2001;Wen & Burne 2004), flagella and motility (Jeon et al, 2003;Schneider et al, 2002;Stroeher et al, 2003), type III secretion systems (Sperandio et al, 1999), toxin production (Ohtani et al, 2002) and virulence (Lyon et al, 2001; Parsonnet et al, 1991;Stroeher et al, 2003).Helicobacter pylori has been identified as the aetiological agent of chronic active gastritis, peptic ulcer disease (Blaser, 1992;Graham, 1989), gastric adenocarcinoma (Parsonnet et al, 1991) and mucosal-associated lymphoid tissue (MALT) lymphoma (Wotherspoon et al, 1993). H. pylori has flagellar motility and is able to move through the Matsumoto et al, 1997;Yokota et al, 1991).…”