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Poster

Session: Session 1 Presenting Authors at Posters (Odds)

P-185 - Investigation of the function(s) of the LuxR solo PsaR3 in Pseudomonas syringae pv. actinidiae: insights into virulence regulation and autoregulation

Monday, July 14, 2025
13:30 - 15:15  
Location: Confex Hall 3
Microbial infection strategies (pathogens & non-pathogens)

    Presenting Author(s)

  • IL

    Ilaria Lucato

    University of Verona
    Morgano, Veneto, Italy

    • Author(s)

  • AR

    Alice Regaiolo

    Johannes Gutenberg-Universität
    Mainz, Rheinland-Pfalz, Germany

  • DD

    Davide Danzi

    University of Verona
    Verona, Veneto, Italy

  • RH

    Ralf Heermann

    Johannes Gutenberg University of Mainz
    Mainz, Rheinland-Pfalz, Germany

  • IB

    Iris Bertani

    ICGEB • Centro Internazionale per l'Ingegneria Genetica e Biotecnologie
    Trieste, Friuli-Venezia Giulia, Italy

  • VV

    Vittorio Venturi

    ICGEB • Centro Internazionale per l'Ingegneria Genetica e Biotecnologie
    Trieste, Friuli-Venezia Giulia, Italy

  • AP

    Annalisa Polverari

    University of Verona
    Verona, Veneto, Italy

  • EV

    Elodie Vandelle

    University of Verona
    Verona, Veneto, Italy


Pseudomonas syringae pv. actinidiae (Psa) causes kiwifruit bacterial canker. The most aggressive biovar, Psa3, carries a plasmid encoding the LuxR solo PsaR3, which may play a role in virulence.


 


A transcriptomic analysis on a strain overexpressing an inducible PsaR3 showed that PsaR3 upregulates genes related to the type III secretion system and flagellar motility, as well as of a plasmid-borne gene cluster, including psaR3 itself.



In this cluster, the two operons are separated by an intergenic region (IR), that we showed to act as a PsaR3-regulated bidirectional promoter. Since no inducer was added to the system, PsaR3 activity may result from (1) the presence of an endogenous signal produced by Psa3 or (2) its autoactivation.



We thus designed a chimeric protein, using the DNA-binding domain of PsaR3 and the autoinducer-binding domain of CviR from Chromobacterium violaceum. The results show that the bacteria expressing the constitutive chimeric protein do not respond to AHLs, backing PsaR3 autoactivation. Moreover, they show a decreased hrpA1 promoter activity, an increased biofilm and siderophore production, correlated with a higher di-c-GMP level. This suggests a desensitization mechanism, in which a negative feedback on PsaR3 function would prevent the constant activation of the virulence. This study highlights LuxR solo function in plant-pathogens interactions and reveals a possible autoactivation mechanism regulating Psa virulence.