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Rapid cell elongation in the primary root and the associated high demand for cell wall biosynthesis makes this tissue particularly vulnerable to cell wall damage. We have established that an active signalling mechanism controls root elongation in response to cell wall perturbation (1). Using microarrays and quantitative phosphoproteomics of young roots treated with inhibitors of cellulose biosynthesis, we have identified putative components of this pathway. Among them is a receptor-like kinase (RLK) with putative extracellular carbohydrate binding domains that is strongly and transiently induced by the inhibitor and that is required for the acute response to cell wall stress.
In this project, K.O. mutants of the RLK and other candidates will be characterised in depth for cell wall-related growth phenotypes and response to cell wall damage. Double mutants between the candidates and with previously identified putative cell wall sensors will be generated to establish genetic interactions and whether one or more pathways for cell wall integrity signalling exist in the root. Molecular and biochemical tools will be used to study the function of potential cell wall sensors, including phosphoproteomic analysis of early cell wall damage signalling in mutants versus wild type. Finally, the impact of defects in cell wall integrity signalling on resistance to biotrophic and necrotrophic pathogens will be analysed.

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