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Medicago truncatula IPD3 Is a Member of the Common Symbiotic Signaling Pathway Required for Rhizobial and Mycorrhizal Symbioses

¹Agricultural Biotechnology Center, Gödöllö 2100, Hungary; ²Department of Agronomy, University of Wisconsin, 1575 Linden Drive, Madison 53706, U.S.A.; ³John Innes Centre, Norwich NR4 7UH, United Kingdom; ⁴Cellular Imaging Laboratory, Biological Research Center, Szeged 6726, Hungary; ⁵Samuel Roberts Noble Foundation, 2510 Sam Noble Parkway, Ardmore, OK 73401, U.S.A.; ⁶Institut des Sciences du Végétal, CNRS, 91198 Gif sur Yvette, France

Legumes form endosymbiotic associations with nitrogen-fixing bacteria and arbuscular mycorrhizal (AM) fungi which facilitate nutrient uptake. Both symbiotic interactions require a molecular signal exchange between the plant and the symbiont, and this involves a conserved symbiosis (Sym) signaling pathway. In order to identify plant genes required for intracellular accommodation of nitrogen-fixing bacteria and AM fungi, we characterized Medicago truncatula symbiotic mutants defective for rhizobial infection of nodule cells and colonization of root cells by AM hyphae. Here, we describe mutants impaired in the interacting protein of DMI3 (IPD3) gene, which has been identified earlier as an interacting partner of the calcium/calmodulin-dependent protein, a member of the Sym pathway. The ipd3 mutants are impaired in both rhizobial and mycorrhizal colonization and we show that IPD3 is necessary for appropriate Nod-factor-induced gene expression. This indicates that IPD3 is a member of the common Sym pathway. We observed differences in the severity of ipd3 mutants that appear to be the result of the genetic background. This supports the hypothesis that IPD3 function is partially redundant and, thus, additional genetic components must exist that have analogous functions to IPD3. This explains why mutations in an essential component of the Sym pathway have defects at late stages of the symbiotic interactions.