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- This is a joint project between the James Hutton Institute (JHI, formerly SCRI) and Rothamsted Research (RRes) that focuses on the "Combating pests and diseases" research challenge highlighted by the industrial members of the Crop Improvement Research Club (CIRC). It is addressing one of the highlighted areas for the second CIRC call: Crop protection. Two teams with complementary expertise in different areas of plant science will combine efforts in exploiting pathogen genome sequence. We aim to advance fundamental understanding of plant immune responses and identify novel sources of resistance to the most economically important barley fungal pathogen Rhynchosporium commune (Rc), formerly known as R. secalis. Rc can cause yield losses of up to 40% and reduce grain quality. Populations of Rc can change rapidly, defeating new barley resistance (R) genes and fungicides after just a few seasons of their widespread commercial use. New EU regulations may lead to loss of the most effective triazole fungicides, making Rc control even more problematic. All pathogens trigger non-host resistance (NHR) in plants. Successful pathogens can suppress or manipulate NHR by secretion of small proteins called 'effectors'. Once a pathogen has suppressed NHR, plants deploy a second layer of defence in the form of R proteins. R proteins detect certain pathogen effectors, termed 'avirulence' (Avr) proteins, and activate resistance responses. Pathogens can avoid recognition by some of the R proteins by losing either the expression or function of a non-essential (redundant) effector with no apparent cost to pathogen fitness. Both of these strategies have been deployed by Rc, mutating or eliminating AvrRrs1, to completely overcome Rrs1-mediated resistance in under 10 years. We aim to understand redundancy within Rc effectors. R proteins recognising non-essential effectors are not durable. Therefore breeding should aim to target introgression of R genes recognising essential effectors that are less variable in pathogen populations. This effector type has been found for other fungal and oomycete plant pathogens. Rc genome sequencing has provided a unique opportunity to identify the putative effector repertoire. Comparison of genome sequences of 9 Rc strains that are able to overcome different R genes will allow rapid prediction of candidate effectors that are less variable in Rc populations, and therefore are more likely to be indispensable. RNA sequencing of Rc germinated conidia and barley leaves infected with Rc provides important information about predicted effectors expressed during the onset of infection. Expression of less variable candidate Rc effectors will be assessed throughout the infection. Based on expression profiles, degree of conservation between the strains, and the ability to induce cell death in one or more barley genotype, 25 predicted effectors will be chosen for targeted gene disruption to identify those essential for fungal pathogenicity. The RRes team has recently developed an efficient system for screening barley germplasm for recognition of Rc effectors. It is based on systemic expression of Rc small secreted proteins in barley leaves using a plant virus as a delivery vector. This method can be extended to other cereals, including wheat, and their pathogens. The extensive JHI collection of barley cultivars, landraces and mapping populations will be screened to (1) identify novel sources of distinct and potentially durable resistances to Rc, which can be combined to increase the durability of resistance, and (2) characterise resistance already present in current breeding material. This will have direct positive impact on Rc disease resistance breeding programmes. Deployment of this resistance will stably increase yield and quality of new barley cultivars, while reducing fungicide use, greenhouse gas emissions and environmental pollution.