Abstract
In Lotus japonicus, a LysM receptor kinase, EPR3, distinguishes compatible and incompatible rhizobial exopolysaccharides at the epidermis. However, the role of this recognition system in bacterial colonization of the root interior is unknown. Here we show that EPR3 advances the intracellular infection mechanism that mediates infection thread invasion of the root cortex and nodule primordia. At the cellular level, Epr3 expression delineates progression of infection threads into nodule primordia and cortical infection thread formation is impaired in epr3 mutants. Genetic dissection of this developmental coordination showed that Epr3 is integrated into the symbiosis signal transduction pathways. Further analysis showed differential expression of Epr3 in the epidermis and cortical primordia and identified key transcription factors controlling this tissue specificity. These results suggest that exopolysaccharide recognition is reiterated during the progressing infection and that EPR3 perception of compatible exopolysaccharide promotes an intracellular cortical infection mechanism maintaining bacteria enclosed in plant membranes.
Highlights
In Lotus japonicus, a LysM receptor kinase, EPR3, distinguishes compatible and incompatible rhizobial exopolysaccharides at the epidermis
In Lotus, both root hair infection and nodule organogenesis pathways are under the control of the LysM-domain-containing Nod factor receptors, NFR1 and NFR5, that trigger two signal transduction pathways following the perception of rhizobial Nod factor signals[9,10,11,12,13]
To assess the role of EPS perception in later stages of the nodule infection process, we traced the consequences of perturbed EPS perception on rhizobial invasion of the root cortex and nodule primordia
Summary
In Lotus japonicus, a LysM receptor kinase, EPR3, distinguishes compatible and incompatible rhizobial exopolysaccharides at the epidermis. Further analysis showed differential expression of Epr[3] in the epidermis and cortical primordia and identified key transcription factors controlling this tissue specificity These results suggest that exopolysaccharide recognition is reiterated during the progressing infection and that EPR3 perception of compatible exopolysaccharide promotes an intracellular cortical infection mechanism maintaining bacteria enclosed in plant membranes. Crack entry between epidermal cells, often associated with lateral root formation, is an alternative intercellular route known from a number of legumes, for example, peanut (Arachis hypogaea), Aeschynomene and Sesbania rostrata[2,3,4] In some of these legumes rhizobia remain intercellular until symbiosomes are formed by endocytosis, whereas in others cortical infection threads develop from the initial infection pockets re-establishing an intracellular entry mode in the root cortex[3]. EPR3 acts in the root cortex and nodule primordia to support and sustain the containment of rhizobia and to facilitate an efficient infection process
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