Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5799947 | Veterinary Microbiology | 2015 | 9 Pages |
â¢Generation of A. pleuropneumoniae QseB/QseC deletion mutant ÎqseBC and PilM mutant ÎpilM.â¢44 differently expressed genes in ÎqseBC were identified by microarray.â¢Direct regulation of PilM by QseB was confirmed by EMSA.â¢PilM mutation leads to reduced adherence ability to SJPL cells.â¢PilM contributes to the pathogenesis in pigs and is an important virulence determinant.
QseB/QseC is one of the five predicted two-component systems (TCSs) in Actinobacillus pleuropneumoniae. To understand the roles of this TCS in A. pleuropneumoniae, a markerless gene-deletion mutant ÎqseBC was constructed. Differentially expressed (DE) genes in ÎqseBC were filtered by microarray analysis. A total of 44 DE genes were found to be regulated by QseB/QseC system. The transcriptional profile of A. pleuropneumoniae ÎqseBC was compared with that of ÎluxS and catecholamine (CA) stimulations, 13 genes regulated by QseB/QseC were found also regulated by LuxS, and 3 Qse-regulons were co-regulated by CA stimulations, respectively. Binding of QseB to the promoters of three regulons (pilM, glpK and hugZ), which were co-regulated by QseB/QseC and LuxS, was evaluated by electrophoretic mobility-shift assay. Results indicated that pilM was directly regulated by phosphorylated-QseB. Then the pilM deletion mutant ÎpilM was constructed and characterized. Data presented here revealed that adherence ability of ÎpilM to St. Jude porcine lung cells was significantly decreased, and ÎpilM exhibited reduced virulence in pigs, suggesting PilM contributes to the process of A. pleuropneumoniae infection.