In nature, plants are challenged by disease-causing pathogens such as viruses, bacteria and fungi. Understanding mechanisms of plant disease and disease resistance is of fundamental importance to sustainable agriculture and human health. Unlike mammals, plants lack a circulating immune system. Plants instead rely on the innate immune capacity of each cell and systemic signals that disseminate from infection sites. Successful pathogens use effectors to suppress plant immunity and cause disease. Plants have evolved disease resistance genes encoding immune receptors that perceive specific pathogen effectors to mount effector-triggered immunity. In Arabidopsis, a heteromeric pair of intracellular immune receptors forms a functional recognition complex which senses virulence activities of two structurally unrelated bacterial effectors at the nuclear chromatin. Results suggest that effector targeting of histone modifications and chromatin remodelling interferes with host basal immunity and that this is transduced by the receptor pair to activation of defence pathways. The underlying molecular mechanisms remain unclear. We have found that the two bacterial effectors interact with an overlapping set of chromatin-associated proteins and with certain immune receptor domains. We hypothesize that the effectors converge on the same chromatin machinery for promoting disease and that their actions are intercepted by the immune receptor system which is physically connected to basal immunity signalling components. By using the effectors as molecular probes, this proposal aims to elucidate how the chromatin environment is modulated during infection and how effector perturbations are converted to effective immunity.
