The suhB gene of Burkholderia cenocepacia is required for protein secretion, biofilm formation, motility and polymyxin B resistance.

Burkholderia cenocepacia is a member of the Burkholderia cepacia complex (Bcc), a group of Gram-negative opportunistic pathogens that cause severe lung infections in patients with cystic fibrosis and display extreme intrinsic resistance to antibiotics, including antimicrobial peptides. B. cenocepacia BCAL2157 encodes a protein homologous to SuhB, an inositol-1-monophosphatase from Escherichia coli, which was suggested to participate in post-transcriptional control of gene expression. In this work we show that a deletion of the suhB-like gene in B. cenocepacia (ΔsuhB(Bc)) was associated with pleiotropic phenotypes. The ΔsuhB(Bc) mutant had a growth defect manifested by an almost twofold increase in the generation time relative to the parental strain. The mutant also had a general defect in protein secretion, motility and biofilm formation. Further analysis of the type II and type VI secretion systems (T2SS and T6SS) activities revealed that these secretion systems were inactive in the ΔsuhB(Bc) mutant. In addition, the mutant exhibited increased susceptibility to polymyxin B but not to aminoglycosides such as gentamicin and kanamycin. Together, our results demonstrate that suhB(Bc) deletion compromises general protein secretion, including the activity of the T2SS and the T6SS, and affects polymyxin B resistance, motility and biofilm formation. The pleiotropic effects observed upon suhB(Bc) deletion demonstrate that suhB(Bc) plays a critical role in the physiology of B. cenocepacia.