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Staphylococcus aureus glucose-induced biofilm accessory proteins, GbaAB, influence biofilm formation in a PIA-dependent manner

Staphylococcus aureus glucose-induced biofilm accessory proteins, GbaAB, influence biofilm formation in a PIA-dependent manner

International Journal of Medical Microbiology 304(5-6): 603-612

The Gram-positive bacteria Staphylococcus aureus and Staphylococcus epidermidis are capable of attaching to a biomaterial surface and forming resistant biofilms. The identification of biomolecular and regulatory factors involved in staphylococcal adhesion and biofilm formation is needed to understand biofilm-associated infection in humans. Here, we have identified a new operon, gbaAB (glucose induced biofilm accessory gene), that affects biofilm formation in S. aureus NCTC8325. Real-time reverse transcription PCR (RT-PCR) and electrophoretic mobility shift assay showed that GbaA and GbaB are transcribed from the same transcript, and GbaA directly inhibits the transcription of the gbaAB operon through self-repression. Our results indicated that the gbaA mutant displayed enhanced biofilm formation compared with the wild type. However, the gbaB and the gbaAB double mutant displayed reduced biofilm formation, suggesting that the gbaAB operon is involved in biofilm formation and that gbaB might be the key gene in biofilm regulation. Phenotypic analysis suggested that the gbaAB operon mediated biofilm formation of S. aureus at the multicellular aggregation stage rather than during initial attachment. In addition, real-time RT-PCR analysis showed that icaA was upregulated in the gbaA mutant and downregulated in the gbaB and gbaAB mutants compared with the wild type. In addition, the gbaA and the gbaB mutants affected the induction of biofilm formation by glucose. Our results suggest that the gbaAB operon is involved in the regulation of the multicellular aggregation step of S. aureus biofilm formation in response to glucose and that this regulation may be mediated through the ica operon.

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Accession: 055906783

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PMID: 24836943

DOI: 10.1016/j.ijmm.2014.04.003

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