The calcium-dependent protein kinase CPK28 negatively regulates the BIK1-mediated PAMP-induced calcium burst |
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Authors: | Jacqueline Monaghan Susanne Matschi Tina Romeis Cyril Zipfel |
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Institution: | 1.The Sainsbury Laboratory; Norwich Research Park; Norwich, United Kingdom;2.Department of Plant Biochemistry; Dahlem Center of Plant Sciences; Freie Universität Berlin; Berlin, Germany;3.Present address: The Sainsbury Laboratory; Norwich Research Park; Norwich, United Kingdom |
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Abstract: | Plants are protected from microbial infection by a robust immune system. Two of the earliest responses mediated by surface-localized immune receptors include an increase in cytosolic calcium (Ca2+) and a burst of apoplastic reactive oxygen species (ROS). The Arabidopsis plasma membrane-associated cytoplasmic kinase BIK1 is an immediate convergent substrate of multiple surface-localized immune receptors that is genetically required for the PAMP-induced Ca2+ burst and directly regulates ROS production catalyzed by the NADPH oxidase RBOHD. We recently demonstrated that Arabidopsis plants maintain an optimal level of BIK1 through a process of continuous degradation regulated by the Ca2+-dependent protein kinase CPK28. cpk28 mutants accumulate more BIK1 protein and display enhanced immune signaling, while plants over-expressing CPK28 accumulate less BIK1 protein and display impaired immune signaling. Here, we show that CPK28 additionally contributes to the PAMP-induced Ca2+ burst, supporting its role as a negative regulator of BIK1. |
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Keywords: | arabidopsis BIK1 CPK28 calcium PAMP-triggered immunity phosphorylation signal transduction |
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