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Research article2013Peer reviewedOpen access

Lack of RsmA-Mediated Control Results in Constant Hypervirulence, Cell Elongation, and Hyperflagellation in Pectobacterium wasabiae

Koiv, Viia; Andresen, Liis; Broberg, Martin; Frolova, Jekaterina; Somervuo, Panu; Auvinen, Petri; Pirhonen, Minna; Tenson, Tanel; Maee, Andres

Abstract

The posttranscriptional regulator RsmA controls the production of plant cell wall degrading enzymes (PCWDE) and cell motility in the Pectobacterium genus of plant pathogens. In this study the physiological role of gene regulation by RsmA is under investigation. Disruption of rsmA gene of the Pectobacterium wasabiae strain, SCC3193 resulted in 3-fold decrease in growth rate and increased virulence. The comparison of mRNA levels of the rsmA(-) mutant and wild-type using a genome-wide microarray showed, that genes responsible for successful infection, i.e. virulence factors, motility, butanediol fermentation, various secretion systems etc. were up-regulated in the rsmA(-) strain. The rsmA(-) strain exhibited a higher propensity to swarm and produce PCWDE compared to the wild-type strain. Virulence experiments in potato tubers demonstrated that in spite of its more efficient tissue maceration, the rsmA(-) strain's ability to survive within the host is reduced and the infection site is taken over by resident bacteria. Taken together, in the absence of RsmA, cells revert to a constitutively infective phenotype characterized by expression of virulence factors and swarming. We hypothesize that lack of control over these costly energetic processes results in decreased growth rate and fitness. In addition, our findings suggest a relationship between swarming and virulence in plant pathogens.

Published in

PLoS ONE
2013, Volume: 8, number: 1, article number: e54248

    UKÄ Subject classification

    Bioinformatics and Systems Biology
    Microbiology
    Genetics

    Publication identifier

    DOI: https://doi.org/10.1371/journal.pone.0054248

    Permanent link to this page (URI)

    https://res.slu.se/id/publ/84933