Phytophthora infestans effector SFI3 targets potato UBK to suppress early immune transcriptional responses

Qin He, Hazel McLellan, Richard K. Hughes, Petra C. Boevink, Miles Armstrong, Yuan Lu, Mark J. Banfield, Zhendong Tian (Lead / Corresponding author), Paul R. J. Birch (Lead / Corresponding author)

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23 Citations (Scopus)
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The potato blight agent Phytophthora infestans secretes a range of RXLR effectors to promote disease. Recent evidence indicates that some effectors suppress early pattern‐triggered immunity (PTI) following perception of Microbe‐Associated Molecular Patterns (MAMPs). Phytophthora infestans effector PiSFI3/Pi06087/PexRD16 was previously shown to suppress MAMP‐triggered pFRK1‐Luciferase reporter gene activity. How PiSFI3 suppresses immunity is unknown.

We employed yeast‐two‐hybrid (Y2H) assays, co‐immunoprecipitation, transcriptional silencing by RNA interference and virus‐induced gene silencing (VIGS), and X‐ray crystallography for structure‐guided mutagenesis, to investigate the function of PiSFI3 in targeting a plant U‐Box‐kinase protein (StUBK) to suppress immunity.

We discovered that PiSFI3 is active in the host nucleus and interacts in yeast and in planta with StUBK. UBK is a positive regulator of specific PTI pathways in both potato and Nicotiana benthamiana. Importantly, it contributes to early transcriptional responses that are suppressed by PiSFI3. PiSFI3 forms an unusual trans‐homodimer. Mutation to disrupt dimerization prevents nucleolar localisation of PiSFI3 and attenuates both its interaction with StUBK and its ability to enhance P. infestans leaf colonisation.

PiSFI3 is a ‘WY domain’ RXLR effector that forms a novel trans‐homodimer which is required for its ability to suppress PTI via interaction with the U‐Box‐kinase protein StUBK.
Original languageEnglish
Pages (from-to)438-454
Number of pages18
JournalNew Phytologist
Issue number1
Early online date10 Dec 2018
Publication statusPublished - Apr 2019


  • potato late blight
  • pathogenicity
  • virulence
  • disease resistance
  • effector-triggered susceptibility


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