Role of tyrosine phosphorylation in the regulation of Burkholderia cell physiology

Abstract

Burkholderia cepacia complex bacteria are opportunistic pathogens, causing severe lung infections in cystic fibrosis patients. Many clinical isolates produce the exopolysaccharide cepacian, believed to be an infection persistence determinant. Little is known about cepacian biosynthesis regulation, but our studies showed the importance of post-translational mechanisms mediated by tyrosine phosphorylation, namely through the tyrosine autokinase BceF, which affects EPS biosynthesis. Indeed, insertion mutants on bceF and bceE genes, this last one encoding an outer membrane porin, caused an exopolysaccharide deficient phenotype, confirming their essential role in EPS biosynthesis. Assessment of biofilm formation showed a stronger reduction in biofilm thickness by the bceF mutant when compared to bceE mutant and the parental strain B. cepacia IST408. Transcriptome analysis suggests that BceF may regulate other cellular functions as indicated by the high number of differentially expressed genes when its transcriptome was compared to the one of the parental strain and the bceE mutant.