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Poster

Session: Session 2 Presenting Authors at Posters (Odds)

P-297 - Using rational design mutations to dissect ɑ-SNAP-Rhg1 function in SCN resistance

Wednesday, July 16, 2025
13:30 - 15:15  
Location: Confex Hall 3
Plant Interactions with nematodes & parasitic plants

    Presenting Author(s)

  • BB

    Benjamin Binstock

    PhD Student
    University of Wisconsin - Madison
    Madison, Wisconsin, United States

    • Author(s)

  • PK

    Paulami Koley

    Postdoctoral Researcher
    University of Wisconsin - Madison
    Madison, Wisconsin, United States

  • AB

    Andrew Bent

    Professor
    University of Wisconsin - Madison
    Madison, Wisconsin, United States

Rhg1 exhibits the strongest known contribution to resistance against soybean cyst nematode (SCN; Heterodera glycines), the most economically damaging pathogen of soybean. Despite progress, our incomplete understanding of Rhg1-dependent resistance limits our ability to engineer improved resistance to SCN as some nematode populations are evolving to partially evade Rhg1 resistance. rhg1-b is a 10-copy haplotype that encodes for three proteins involved in SCN resistance, one of which is an α-SNAP. α-SNAP is a core housekeeping protein of eukaryotic cells that works with NSF (N-ethylmaleimide-Sensitive Factor) to mediate the disassembly and reuse of SNARE proteins, which mediate vesicle fusion to target membranes. The resistance-conferring α-SNAPrhg1-b differs from wild-type α-SNAP due to polymorphisms in 4 of the last 5 residues of the C-terminus, an otherwise highly conserved motif across eukaryotic α-SNAPs that directly participates in binding NSF. These polymorphisms alter SNAP/NSF interaction, interfering with vesicle trafficking and causing localized cytotoxicity in syncytial cells, which defeats SCN. Previous work using N. benthamiana has suggested that mutagenesis of certain residues at the C-terminus of α-SNAPrhg1-b can reduce cytotoxicity, or increase it to a significantly greater level. Some mutations may also restore efficacy against SCN that partially evade Rhg1 resistance. Analysis of multiple C-terminus mutant α-SNAPs both in vivo and in vitro will be presented.