The calcium-dependent protein kinase CPK28 negatively regulates the BIK1-mediated PAMP-induced calcium burst

Jacqueline Monaghan, Susanne Matschi, Tina Romeis, Cyril Zipfel

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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 (Ca(2+)) 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 Ca(2+) 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 Ca(2+)-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 Ca(2+) burst, supporting its role as a negative regulator of BIK1.

Original languageEnglish
Article numbere1018497
Number of pages5
JournalPlant Signaling & Behavior
Volume10
Issue number5
Early online date3 Jun 2015
DOIs
Publication statusPublished - 2015

Keywords

  • arabidopsis
  • BIK1
  • CPK28
  • calcium
  • PAMP-triggered immunity
  • phosphorylation
  • signal transduction

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