Protein phosphatase AP2C1 negatively regulates basal resistance and defense responses to Pseudomonas syringae

Volodymyr Shubchynskyy, Justyna Boniecka, Alois Schweighofer, Justinas Simulis, Kotryna Kvederaviciute, Michael Stumpe, Felix Mauch, Salma Balazadeh, Bernd Mueller-Roeber, Freddy Boutrot, Cyril Zipfel, Irute Meskiene

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Abstract

Mitogen-activated protein kinases (MAPKs) mediate plant immune responses to pathogenic bacteria. However, less is known about the cell autonomous negative regulatory mechanism controlling basal plant immunity. We report the biological role of Arabidopsis thaliana MAPK phosphatase AP2C1 as a negative regulator of plant basal resistance and defense responses to Pseudomonas syringae AP2C2, a closely related MAPK phosphatase, also negatively controls plant resistance. Loss of AP2C1 leads to enhanced pathogen-induced MAPK activities, increased callose deposition in response to pathogen-associated molecular patterns or to P. syringae pv. tomato (Pto) DC3000, and enhanced resistance to bacterial infection with Pto. We also reveal the impact of AP2C1 on the global transcriptional reprogramming of transcription factors during Pto infection. Importantly, ap2c1 plants show salicylic acid-independent transcriptional reprogramming of several defense genes and enhanced ethylene production in response to Pto This study pinpoints the specificity of MAPK regulation by the different MAPK phosphatases AP2C1 and MKP1, which control the same MAPK substrates, nevertheless leading to different downstream events. We suggest that precise and specific control of defined MAPKs by MAPK phosphatases during plant challenge with pathogenic bacteria can strongly influence plant resistance.

Original languageEnglish
Pages (from-to)1169-1183
JournalJournal of Experimental Botany
Volume68
Issue number5
Early online date6 Jan 2017
DOIs
Publication statusPublished - 1 Feb 2017

Keywords

  • Callose
  • defense genes
  • MAPK
  • MAPK phosphatase
  • PAMP
  • PP2C phosphatase
  • Pseudomonas syringae
  • salicylic acid
  • transcription factors

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