Abstract
Soybean (Glycine max) plants counteract soybean cyst nematode (SCN, Heterodera glycines Ichinohe) infection through an impairment of soluble N-ethylmaleimide-sensitive factor (NSF) attachment protein (α-SNAP) - NSF interactions and vesicular trafficking leading to cellular toxicity in response to nematode feeding. Through the use of a bi-parental mapping population from a cross between the SCN-resistant soybean cultivars Pickett × Peking, a major QTL on chromosome 14 was mapped to a confidence interval containing the GmSNAP14 gene. SCN-resistant genotypes were found to carry one of two variant GmSNAP14 alleles harboring either a deletion or an insertion in GmSNAP14. Expression of full-length transcripts was absent or markedly lower in plants carrying these alleles when compared to susceptible plants. Additionally, the generation of deleted and/or alternatively spliced isoforms coding for GmSNAP14 C-terminal variant proteins was pronounced in resistant plants, suggesting that SCN resistance may result from a combination of diminished GmSNAP14 expression and GmSNAP14 protein variants. CRISPR/Cas9-mediated knockout of GmSNAP14 enhanced resistance to SCN, consistent with susceptibility gene behavior indicating GmSNAP14 as a potential nematode virulence target. Our findings can be leveraged through the use of genome editing and conventional breeding techniques utilizing native alleles to develop resistant soybean cultivars.