Soybean Cyst Nematode Resistance Quantitative Trait Locus Alters the Expression of a γ-SNAP Protein.

Soybean cyst nematode (SCN) is the most economically damaging pathogen of soybean and host resistance is a core management strategy. The SCN resistance quantitative trait locus , introgressed from the wild relative , provides intermediate resistance against nematode populations, including those with increased virulence on the heavily used resistance locus. was previously fine-mapped to a genome interval on chromosome 15. The present study determined that at , encoding a γ-SNAP, contributes to SCN resistance. CRISPR/Cas9-mediated disruption of the allele reduced SCN resistance in transgenic roots. There are no encoded amino acid polymorphisms between resistant and susceptible alleles. However, other -specific DNA polymorphisms in the promoter and gene body were identified, and we observed differing induction of γ-SNAP protein abundance at SCN infection sites between resistant and susceptible roots. We identified alternative RNA splice forms transcribed from the γ-SNAP gene and observed differential expression of the splice forms 2 days after SCN infection. Heterologous overexpression of γ-SNAPs in plant leaves caused moderate necrosis, suggesting that careful regulation of this protein is required for cellular homeostasis. Apparently, certain evolved quantitative SCN resistance through altered regulation of γ-SNAP. Previous work has demonstrated SCN resistance impacts of the soybean α-SNAP proteins encoded by () and . The present study shows that a different type of SNAP protein can also impact SCN resistance. Little is known about γ-SNAPs in any system, but the present work suggests a role for γ-SNAPs during susceptible responses to cyst nematodes.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.