Concurrent Session
Tifaine Folletti
Laboratoire des Interactions Plantes-Microbes-Environnement (LIPME), Université de Toulouse, INRAE, CNRS
Castanet Tolosan, Midi-Pyrenees, France
Sophie Massot
Université Paris Cité, CNRS, INRAE, Institute of Plant Sciences Paris-Saclay, 91190 Gif sur Yvette, France
Gif sur Yvette, Ile-de-France, France
Laurent Sauviac
Laboratoire des Interactions Plantes-Microbes-Environnement (LIPME), Université de Toulouse, INRAE, CNRS
Castanet Tolosan, Midi-Pyrenees, France
Fabienne Vailleau
Director
Laboratoire des Interactions Plantes-Microbes-Environnement (LIPME), Université de Toulouse, INRAE, CNRS
Castanet Tolosan, Midi-Pyrenees, France
Jörn Piel
Institute of Microbiology, Eidgenössische Technische Hochschule Zurich
Zurich, Zurich, Switzerland
Pascal Ratet
Université Paris-Saclay, CNRS, INRAE, Université Evry, Institute of Plant Sciences Paris-Saclay
Gif sur Yvette, Ile-de-France, France
Benjamin Gourion
Laboratoire des Interactions Plantes-Microbes-Environnement (LIPME), Université de Toulouse, INRAE, CNRS
Castanet Tolosan, Midi-Pyrenees, France
The frontiers between pathogenic and mutualistic organisms are sometimes blurry. We have recently characterized a clade of atypical rhizobia that trigger plant death on young seedlings and nodulation on older plants of the same species. The virulence factors involved in the pathogenic interactions were not known. To identify them, we exploited the diversity of the Ensifer adhaerens species and looked for specificities shared by pathogenic strains and absent in non-pathogenic ones. We thus performed comparative genomics that led us to investigate the role of a 200kbp plasmid harboring 34% of CDS specific to the pathogenic strains. We identified on this plasmid a 70kb region that includes a biosynthetic gene cluster (BGC) that likely encodes for polyketide synthases. Computational biology predicted that the BGC might be responsible for the production of spliceostatin, a toxin that inhibits the spliceosome. We constructed mutants deleted for this BGC in the T4 strain, the model bacterium of this clade. Plant inoculations revealed that the deletion mutant was totally avirulent suggesting that this BGC is crucial for virulence. We then confirmed the role of this BGC by constructing a deletion mutant that displayed the same avirulent phenotype in T173, another strain of this clade. Together our data indicate that the spliceostatin BGC is the key factor of pathogenicity in this atypical clade of rhizobia, triggering nodulation on developed plant and plant death on young seedlings.