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<p>The wheat resistance gene <i>Pm4</i> encodes a kinase fusion protein and has gained particular attention as it confers race-specific resistance against two major wheat pathogens: powdery mildew and blast. Here we describe the identification of AvrPm4, the mildew avirulence effector recognized by Pm4, using UV mutagenesis, and its functional validation in wheat protoplasts. We show that AvrPm4 directly interacts with and is phosphorylated by Pm4. Using genetic association and quantitative trait locus mapping, we further demonstrate that the evasion of <i>Pm4</i> resistance by virulent mildew isolates relies on a second fungal component, <i>SvrPm4</i>, which suppresses <i>AvrPm4</i>-induced cell death. Surprisingly, <i>SvrPm4</i> was previously described as <i>AvrPm1a</i>. We show that SvrPm4, but not its inactive variant svrPm4, is recognized by the nucleotide-binding leucine-rich repeat immune receptor Pm1a. These multiple roles of a single effector provide a new perspective on fungal (a)virulence proteins and their combinatorial interactions with different types of immune receptors.</p>

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Virulence on Pm4 kinase-based resistance is determined by two divergent wheat powdery mildew effectors

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月12日

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  • Zoe Bernasconi,
  • Aline G. Herger,
  • Maria Del Pilar Caro,
  • Lukas Kunz,
  • Marion C. Müller,
  • Ursin Stirnemann,
  • Megan A. Outram,
  • Victoria Widrig,
  • Matthias Neidhart,
  • Jonatan Isaksson,
  • Seraina Schudel,
  • Sebastian Rösli,
  • Thomas Wicker,
  • Kyle W. Bender,
  • Cyril Zipfel,
  • Peter N. Dodds,
  • Melania Figueroa,
  • Javier Sánchez-Martín,
  • Beat Keller

摘要

The wheat resistance gene Pm4 encodes a kinase fusion protein and has gained particular attention as it confers race-specific resistance against two major wheat pathogens: powdery mildew and blast. Here we describe the identification of AvrPm4, the mildew avirulence effector recognized by Pm4, using UV mutagenesis, and its functional validation in wheat protoplasts. We show that AvrPm4 directly interacts with and is phosphorylated by Pm4. Using genetic association and quantitative trait locus mapping, we further demonstrate that the evasion of Pm4 resistance by virulent mildew isolates relies on a second fungal component, SvrPm4, which suppresses AvrPm4-induced cell death. Surprisingly, SvrPm4 was previously described as AvrPm1a. We show that SvrPm4, but not its inactive variant svrPm4, is recognized by the nucleotide-binding leucine-rich repeat immune receptor Pm1a. These multiple roles of a single effector provide a new perspective on fungal (a)virulence proteins and their combinatorial interactions with different types of immune receptors.