Transcriptomic analysis reveals a novel LysR regulator's role in Burkholderia pseudomallei host-pathogen interaction
- PMID: 41033370
- DOI: 10.1016/j.micpath.2025.108078
Transcriptomic analysis reveals a novel LysR regulator's role in Burkholderia pseudomallei host-pathogen interaction
Abstract
Burkholderia pseudomallei is a Gram-negative pathogen responsible for melioidosis, a life-threatening disease endemic to Southeast Asia. LysR-type transcriptional regulators (LTTRs) are known key regulators of bacterial pathogenesis and metabolism, yet many remain uncharacterized. This study investigates the function of UKMD286_5923, a novel LTTR, in B. pseudomallei UKMD286. We constructed a deletion mutant and performed transcriptomic analysis via RNA sequencing. This analysis identified 67 differentially expressed genes, with 45 genes upregulated and 22 genes downregulated in the mutant compared to the wild-type. Functional enrichment analysis of these genes highlighted significant roles in metabolism, transport and secretion system. To further characterize the phenotypic impact of the gene deletion, we conducted biofilm formation and plaque assays. Biofilm formation assays showed increased biofilm production in the mutant, suggesting a regulatory role in bacterial adhesion. Plaque assays revealed reduced plaque formation in the mutant, indicating impaired host cell invasion. These findings collectively suggest that UKMD286_5923 influences genes essential for bacterial survival and host-pathogen interaction, including components of the Type III secretion system. Understanding the function of this regulator enhances our knowledge of B. pseudomallei pathogenesis and may contribute to future diagnostic and treatment strategies for melioidosis.
Copyright © 2025 Elsevier Ltd. All rights reserved.
Conflict of interest statement
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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