4.8 Article

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

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NATURE COMMUNICATIONS
卷 7, 期 -, 页码 -

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NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms10311

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资金

  1. Biotechnology and Biological Sciences Research Council (BBSRC) [BB/G015244/1, BB/K018183/1, BB/L026880/1]
  2. Scottish Government Rural and Environment Science and Analytical Services Division (RESAS)
  3. China Scholarship Council (CSC)
  4. Doctoral Fund of the Ministry of Education of China [20110146110019]
  5. James Hutton Institute SEEDCORN initiative
  6. BBSRC [BB/K018299/1, BB/N009967/1, BB/L008025/1, BB/L026880/1, BB/G015244/1] Funding Source: UKRI
  7. Biotechnology and Biological Sciences Research Council [BB/K018299/1, BB/G015244/1, BB/L008025/1, BB/L026880/1, BB/K018183/1, BB/N009967/1] Funding Source: researchfish

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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.

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