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A Phytophthora infestans RXLR effector targets plant PP1c isoforms that promote late blight disease

Author

Listed:
  • Petra C. Boevink

    (James Hutton Institute)

  • Xiaodan Wang

    (James Hutton Institute
    College of Life Science, University of Dundee (at JHI)
    Virus-free Seedling Research Institute of Heilongjiang Academy of Agricultural Sciences)

  • Hazel McLellan

    (College of Life Science, University of Dundee (at JHI))

  • Qin He

    (College of Life Science, University of Dundee (at JHI)
    Key Laboratory of Horticultural Plant Biology (at HAU), Ministry of Education, National Center for Vegetable Improvement (Central China), Huazhong Agricultural University)

  • Shaista Naqvi

    (James Hutton Institute)

  • Miles R. Armstrong

    (James Hutton Institute
    College of Life Science, University of Dundee (at JHI))

  • Wei Zhang

    (Key Laboratory of Horticultural Plant Biology (at HAU), Ministry of Education, National Center for Vegetable Improvement (Central China), Huazhong Agricultural University)

  • Ingo Hein

    (James Hutton Institute)

  • Eleanor M. Gilroy

    (James Hutton Institute)

  • Zhendong Tian

    (Key Laboratory of Horticultural Plant Biology (at HAU), Ministry of Education, National Center for Vegetable Improvement (Central China), Huazhong Agricultural University)

  • Paul R. J. Birch

    (James Hutton Institute
    College of Life Science, University of Dundee (at JHI))

Abstract

Plant pathogens deliver effectors to alter host processes. Knowledge of how effectors target and manipulate host proteins is critical to understand crop disease. Here, we show that in planta expression of the RXLR effector Pi04314 enhances leaf colonization by Phytophthora infestans via activity in the host nucleus and attenuates induction of jasmonic and salicylic acid-responsive genes. Pi04314 interacts with three host protein phosphatase 1 catalytic (PP1c) isoforms, causing their re-localization from the nucleolus to the nucleoplasm. Re-localization of PP1c-1 also occurs during infection and is dependent on an R/KVxF motif in the effector. Silencing the PP1c isoforms or overexpression of a phosphatase-dead PP1c-1 mutant attenuates infection, demonstrating that host PP1c activity is required for disease. Moreover, expression of PP1c–1mut abolishes enhanced leaf colonization mediated by in planta Pi04314 expression. We argue that PP1c isoforms are susceptibility factors forming holoenzymes with Pi04314 to promote late blight disease.

Suggested Citation

  • Petra C. Boevink & Xiaodan Wang & Hazel McLellan & Qin He & Shaista Naqvi & Miles R. Armstrong & Wei Zhang & Ingo Hein & Eleanor M. Gilroy & Zhendong Tian & Paul R. J. Birch, 2016. "A Phytophthora infestans RXLR effector targets plant PP1c isoforms that promote late blight disease," Nature Communications, Nature, vol. 7(1), pages 1-14, April.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10311
    DOI: 10.1038/ncomms10311
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    Cited by:

    1. Hui Sheng & Congcong Ai & Cancan Yang & Chunyuan Zhu & Zhe Meng & Fengzhi Wu & Xiaodan Wang & Daolong Dou & Paul F. Morris & Xiuguo Zhang, 2024. "A conserved oomycete effector RxLR23 triggers plant defense responses by targeting ERD15La to release NbNAC68," Nature Communications, Nature, vol. 15(1), pages 1-23, December.

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