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Differential regulation of the Epr3 receptor coordinates membrane-restricted rhizobial colonization of root nodule primordia.


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.

SUBMITTER: Kawaharada Y 

PROVIDER: S-EPMC5331223 | biostudies-literature | 2017 Feb

REPOSITORIES: biostudies-literature

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Differential regulation of the Epr3 receptor coordinates membrane-restricted rhizobial colonization of root nodule primordia.

Kawaharada Yasuyuki Y   Nielsen Mette W MW   Kelly Simon S   James Euan K EK   Andersen Kasper R KR   Rasmussen Sheena R SR   Füchtbauer Winnie W   Madsen Lene H LH   Heckmann Anne B AB   Radutoiu Simona S   Stougaard Jens J  

Nature communications 20170223


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 a  ...[more]

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