ArticleJournal of advanced research2026
Interaction of the polar localization protein BscR with phosphodiesterase PipA regulates virulence strategies in Pseudomonas aeruginosa.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
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Authors and funding
9 authors.
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No grant is acknowledged in the PubMed record.
Abstract
introductionBacteria synthesize cyclic diguanylate monophosphate (c-di-GMP) as a central second messenger to control multiple virulence-related phenotypes. In P. aeruginosa, while the major function of phosphodiesterases and diguanylate cyclases involves controlling cellular c-di-GMP concentrations, the exact pathways through which these enzymes mediate virulence expression are not fully understood.
objectivesWe aimed to identify interacting partners of phosphodiesterase PipA and elucidate their coordination with PipA in regulating bacterial virulence strategies.
methodsWe employed co-immunoprecipitation and bacterial two-hybrid assays to identify BscR as an interacting partner of PipA. Our systematic investigation combining targeted gene disruption, phenotypic screening, and subcellular protein tracking revealed the regulatory network through which BscR and PipA govern bacterial virulence programs. Finally, we evaluated how BscR influences bacterial pathogenicity using cell infection and Galleria mellonella infection models.
resultsOur findings demonstrate that BscR deletion leads to significant reductions in biofilm formation and pyocyanin production, while enhancing bacterial motility. We further reveal that PipA modulates biofilm formation and motility through a BscR-dependent regulatory pathway. Notably, BscR and CheB exhibit co-localization at the cellular poles, with BscR's polar localization requiring direct interaction with CheB. Importantly, we discovered that elevated PipA levels disrupt the BscR-CheB interaction, thereby attenuating BscR-mediated regulatory functions. Furthermore, BscR mutation significantly enhances bacterial virulence, as evidenced by increased cytotoxicity in A549 cell infection and Galleria mellonella infection assays.
conclusionThese findings elucidate that BscR in P. aeruginosa serves as a crucial regulatory factor in modulating bacterial virulence determinants. This study provides mechanistic insights into BscR-mediated virulence regulation, offering a framework to design innovative approaches targeting infection control.
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