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Poster

Session: Session 1 Presenting Authors at Posters (Evens)

P-440 - Resurrection of the Plant Immune Receptor Sr50 to Overcome Pathogen Immune Evasion

Tuesday, July 15, 2025
09:55 - 11:30  
Location: Confex Hall 3
Structure Informed Synthetic Biology: From Design to Function

    Presenting Author(s)

  • KS

    Kyungyong Seong

    University of California, Berkeley
    Berkeley, CA, USA

    • Author(s)

  • WW

    Wei Wei

    Postdoctoral fellow
    University of California, Berkeley
    Berkeley, California, United States

  • SS

    Sophie C. Sent

    Institute for Plant Sciences, University of Cologne
    Cologne, Nordrhein-Westfalen, Germany

  • BV

    Brandon Vega

    University of California, Berkeley
    Berkeley, California, United States

  • AD

    Amanda Dee

    University of California, Berkeley
    Berkeley, California, United States

  • GR

    Griselda Ramirez-Bernardino

    University of California, Berkeley
    Berkeley, California, United States

  • RK

    Rakesh Kumar

    University of California, Berkeley
    Berkeley, California, United States

  • LP

    Lorena Parra

    University of California, Berkeley
    Berkeley, California, United States

  • IS

    Isabel Saur

    Group leader
    University of Cologne, CEPLAS
    Cologne, Nordrhein-Westfalen, Germany

  • KK

    Ksenia Krasileva, PhD (she/her/hers)

    University of California, Berkeley
    Berkeley, CA, USA

The introgression of intracellular nucleotide-binding leucine-rich repeat receptor (NLR) genes into elite crop cultivars is a common strategy for disease control, yet pathogens rapidly evolve to evade NLR-mediated immunity. The NLR gene Sr50 protects wheat against stem rust caused by the fungal pathogen Puccinia graminis f. sp. tritici (Pgt). However, mutations in AvrSr50 allowed Pgt to evade Sr50 recognition, leading to resistance breakdown. Here, we combined iterative computational structural analyses and site-directed mutagenesis to engineer Sr50 recognition of the escape mutant AvrSr50QCMJC. Derived by molecular docking, our initial structural model identified the K711D substitution in Sr50, which partially restored AvrSr50QCMJC recognition. Enhancing Sr50K711D expression via strong promoters compensated for weak recognition and restored robust immune responses. Further structural refinements led to the generation of five double and two triple receptor mutants absent in nature but showing robust dual recognition for AvrSr50 and AvrSr50QCMJC. Notably, the K711D substitution was essential and epistatic to the additional substitutions for AvrSr50QCMJC recognition. Furthermore, this single substitution altered AlphaFold 2 predictions, enabling accurate modeling of the Sr50K711D–AvrSr50 complex structure. Collectively, this study outlines a framework for NLR engineering to counteract pathogen adaptation and provides novel Sr50 variants with potential for stem rust resistance.