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RNAseq of Burkholderia pseudomallei TctR mutant, a regulator of type VI secretion

ABSTRACT: We report the transcriptome of Burkholderia pseudomallei type VI secretion regulator TctR mutant grown in rich media compared to wild type. The RNA-seq studies confirmed the role of TctR as a negative regulator of T6SS-2, a positive regulator of T6SS-6 and suggest a potential role in regulation of the T6SS-3 and T6SS-4 gene clusters.

ORGANISM(S): Burkholderia pseudomallei

PROVIDER: GSE104716 | GEO | 2017/10/09

SECONDARY ACCESSION(S): PRJNA413621

REPOSITORIES: GEO

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RNAseq of Burkholderia pseudomallei TctR mutant, a regulator of type VI secretion

Project description:RNAseq of Burkholderia pseudomallei TctR mutant, a regulator of type VI secretion

| PRJNA413621 | ENA

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Project description:Melioidosis is a disease caused by the Gram-negative bacillus Burkholderia pseudomallei (Bpm), commonly found in soil and water of endemic areas. Naturally acquired human melioidosis infections can result from either exposure through percutaneous inoculation, inhalation, or ingestion of soil-contaminated food or water. Our prior studies recognized Bpm as an effective enteric pathogen, capable of establishing acute or chronic gastrointestinal infections following oral inoculation (Sanchez-Villamil, Tapia et al. 2020). However, the specific mechanisms and virulence factors involved in the pathogenesis of Bpm during intestinal infection are unknown. In our current study, we standardized an in vitro intestinal infection model using mouse primary intestinal epithelial cells (mIECs) and demonstrated that Bpm requires a functional T6SS for full virulence. Further, we performed dual RNA-seq analysis on Bpm-infected mIECs to evaluate differentially expressed host and bacterial genes in the presence or absence of a T6SS. Our results showed a dysregulation in the TNF- signaling via NF-B pathway in the absence of the T6SS, with some of the genes involved in inflammatory processes and cell death also affected. Analysis of the bacterial transcriptome identified virulence factors and regulatory proteins playing a role during infection, with association to the T6SS. By using a Bpm transposon mutant library and isogenic mutants, we showed that deletion of the bicA gene, encoding a putative T3SS/T6SS regulator, ablated intracellular survival and plaque formation by Bpm and impacted survival and virulence when using murine models of acute and chronic gastrointestinal infection. Overall, these results highlight the importance of the type 6 secretion system in the gastrointestinal pathogenesis of Bpm.

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Effect of Mip inhibition on J774A.1 macrophage immune response during Burkholderia pseudomallei infection

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