Mutability in <em>Pseudomonas viridiflava</em> as a programmed balance between antibiotic resistance and pathogenicity

We thank the staff of the INRAE Experimental facilities of the Plant Pathology research unit (IEPV, https://doi.org/10.15454/8DGF-QF70) for their involvement in field experiments

International audience

English. Mutable bacterial cells are defective in their DNA repair system and they often have a phenotype different than their wild-type counterparts. In human bacterial pathogens, the mutable and hypermutable phenotype are often associated with general antibiotic resistance. Here, we quantified the occurrence of mutable cells in <em>Pseudomonas viridiflava</em>, a phytopathogenic bacterium in the <em>P. syringae</em> complex with a broad host range and capacity to live as saprophyte. Two phenotypic variants (transparent and mucoid) were produced by this bacterium. The transparent variant had a mutator phenotype, showed general antibiotic resistance and could not induce disease on the plant species tested (bean). In contrast, the mucoid variant did not display mutability nor resistance to antibiotics and was capable of inducing disease on bean. Both the transparent and mucoid variants were less fit when grown in vitro, while in planta both of the variants and wild-types attained similar population densities. Given the importance of the methyl-directed mismatch repair system (MMR) in the occurrence of mutable and hypermutable cells in human bacterial pathogens, we investigated whether mutations in mut genes were associated with mutator transparent cells in P. viridiflava. Our results showed no mutations in MMR genes in any of the<em> P. viridiflava</em> cells tested. Here we report that high mutation rate and antibiotic resistance are inversely correlated with pathogenicity in P. viridiflava but are not associated with mutations in MMR. In addition,<em> P. viridiflava</em> variants differ from variants produced by other phytopathogenic bacteria in the absence of reversion to the wild-type phenotype.