<i>Sinorhizobium meliloti</i> succinylated high‐molecular‐weight succinoglycan and the <i>Medicago truncatula</i> LysM receptor‐like kinase MtLYK10 participate independently in symbiotic infection

  • Fabienne Maillet
    LIPM Université de Toulouse, INRA, CNRS Castanet‐Tolosan CS 52627 France
  • Joëlle Fournier
    LIPM Université de Toulouse, INRA, CNRS Castanet‐Tolosan CS 52627 France
  • Hajeewaka C. Mendis
    Department of Biological Science Florida State University Tallahassee FL 32306 USA
  • Million Tadege
    Department of Plant and Soil Sciences Institute for Agricultural Biosciences Oklahoma State University Ardmore OK 73401 USA
  • Jiangqi Wen
    Noble Research Institute LLC. 2510 Sam Noble Parkway Ardmore OK 73401 USA
  • Pascal Ratet
    IPS2 Institute of Plant Sciences Paris-Saclay IPS2, CNRS, INRA, Université Paris-Sud, Université Evry, Université Paris-Saclay Bâtiment 630 91405 Orsay France
  • Kirankumar S. Mysore
    Noble Research Institute LLC. 2510 Sam Noble Parkway Ardmore OK 73401 USA
  • Clare Gough
    LIPM Université de Toulouse, INRA, CNRS Castanet‐Tolosan CS 52627 France
  • Kathryn M. Jones
    Department of Biological Science Florida State University Tallahassee FL 32306 USA

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<jats:title>Summary</jats:title><jats:p>The formation of nitrogen‐fixing nodules on legume hosts is a finely tuned process involving many components of both symbiotic partners. Production of the exopolysaccharide succinoglycan by the nitrogen‐fixing bacterium <jats:italic>Sinorhizobium meliloti</jats:italic> 1021 is needed for an effective symbiosis with <jats:italic>Medicago</jats:italic> spp., and the succinyl modification to this polysaccharide is critical. However, it is not known when succinoglycan intervenes in the symbiotic process, and it is not known whether the plant lysin‐motif receptor‐like kinase MtLYK10 intervenes in recognition of succinoglycan, as might be inferred from work on the <jats:italic>Lotus japonicus</jats:italic> MtLYK10 ortholog, LjEPR3. We studied the symbiotic infection phenotypes of <jats:italic>S. meliloti</jats:italic> mutants deficient in succinoglycan production or producing modified succinoglycan, in wild‐type <jats:italic>Medicago truncatula</jats:italic> plants and in <jats:italic>Mtlyk10</jats:italic> mutant plants. On wild‐type plants, <jats:italic>S. meliloti</jats:italic> strains producing no succinoglycan or only unsuccinylated succinoglycan still induced nodule primordia and epidermal infections, but further progression of the symbiotic process was blocked. These <jats:italic>S. meliloti</jats:italic> mutants induced a more severe infection phenotype on <jats:italic>Mtlyk10</jats:italic> mutant plants. Nodulation by succinoglycan‐defective strains was achieved by <jats:italic>in trans</jats:italic> rescue with a Nod factor‐deficient <jats:italic>S. meliloti</jats:italic> mutant. While the Nod factor‐deficient strain was always more abundant inside nodules, the succinoglycan‐deficient strain was more efficient than the strain producing only unsuccinylated succinoglycan. Together, these data show that succinylated succinoglycan is essential for infection thread formation in <jats:italic>M. truncatula</jats:italic>, and that MtLYK10 plays an important, but different role in this symbiotic process. These data also suggest that succinoglycan is more important than Nod factors for bacterial survival inside nodules.</jats:p>

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