Functionally antagonistic integrated domains of the Rpg5 NLR immunity receptor interact to regulate stem rust resistance in barley

Primary author: Shyam Solanki
Co-author(s): Gazala Ameen; Deepika Arora; Pawel Borowicz; Robert Brueggeman
Faculty sponsor: Robert S Bruggeman

Primary college/unit: Agricultural, Human and Natural Resource Sciences
Campus: Pullman

Abstract:

Immunity is important for plants to protect themselves from pathogens. Immunity activation relies on perception of pathogen molecules or by changes they induce to colonize the host tissues. The molecules/proteins pathogens manipulate are susceptibility targets encoded by vulnerable regions of the genome that are under selective pressure by the pathogen. A new paradigm of plant immune receptor evolution suggests plant genome reorganization directed by the pressure exerted by pathogens leading to gene fusion of these susceptibility targets with NLR plant immunity receptors resulting in integrated domains (IDs) that act as pathogen ‘bait-proteins’. These NLR-ID baits allow plants to monitor pathogen induced changes in the host. We identified a barley NLR immune receptor Rpg5 containing a serine threonine kinase (STPK) ID that confers resistance against Puccinia graminis f. sp. tritici (Pgt), the stem rust pathogen. The Rpg5-STPK-ID progenitor, PRK1, an Arabidopsis stomatal kinase AtAPK1b ortholog was hypothesized as important for stomata opening during respiration. Confocal microscopy showed Pgt host entry through stomata in the dark expelling the current dogma that a light period is required for stomata opening and pathogen entry, suggesting stomatal manipulation by Pgt possibly targeting PRK1 to enter the host during the night when the stomates are closed. We hypothesize that the pathogen manipulates PRK1 to open the stomata and enter in the host at night when Pgt spores adapted to germinate, thus forcing the host to evolve the Rpg5-STPK NLR-ID which recognizes the pathogen’s attempt to manipulate PRK1 leading to the activation of plant defense responses.