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

Roberto Rosales-Reyes, Maria Soledad Saldias, Daniel F Aubert, Omar M El-Halfawy, Miguel A Valvano

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

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 posttranscriptional control of gene expression. In this work we show that a deletion of the suhB-like gene in B. cenocepacia (?suhBBc) was associated with pleiotropic phenotypes. The ?suhBBc mutant had a growth defect manifested by an almost 2-fold 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-2 and the Type-6 secretion systems activities revealed that these secretion systems were inactive in the ?suhBBc mutant. In addition, the mutant exhibited increased susceptibility to polymyxin B but not to aminoglycosides like gentamicin and kanamycin. Together, our results demonstrate that suhBBc deletion compromises general protein secretion including the activity of T2SS and T6SS, and affects polymyxin B resistance, motility, and biofilm formation. The pleiotropic effects observed upon suhBBc deletion demonstrate that suhBBc plays a critical role in the physiology of B. cenocepacia.
Original languageEnglish
Pages (from-to)2315-2324
Number of pages10
JournalMicrobiology (Reading, England)
Volume158
Issue number9
DOIs
Publication statusPublished - Sep 2012

ASJC Scopus subject areas

  • Microbiology

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