TheBurkholderia cenocepaciasensor kinase hybrid AtsR is a global regulator modulating quorum-sensing signalling


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Abstract

SummaryBurkholderia cenocepaciais commonly found in the environment and also as an important opportunistic pathogen infecting patients with cystic fibrosis. Successful infection by this bacterium requires coordinated expression of virulence factors, which is achieved through different quorum sensing (QS) regulatory systems. Biofilm formation and Type 6 secretion system (T6SS) expression inB. cenocepaciaK56-2 are positively regulated by QS and negatively regulated by the sensor kinase hybrid AtsR. This study reveals that in addition to affecting biofilm and T6SS activity, the deletion ofatsRinB. cenocepacialeads to overproduction of other QS-regulated virulence determinants including proteases and swarming motility. Expression of the QS genes,cepIRandcciIR, was upregulated in the ΔatsRmutant and resulted in early and increasedN-acylhomoserine lactone (AHL) production, suggesting that AtsR plays a role in controlling the timing and fine-tuning of virulence gene expression by modulating QS signalling. Furthermore, a ΔatsRΔcepIΔcciImutant could partially upregulate the same virulence determinants indicating that AtsR also modulates the expression of virulence genes by a second mechanism, independently of any AHL production. Together, our results strongly suggest that AtsR is a global virulence regulator inB. cenocepacia.

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