The <i>rhg1‐a</i> ( <i>Rhg1</i> low‐copy) nematode resistance source harbors a copia‐family retrotransposon within the <i>Rhg1‐</i> encoded α‐SNAP gene

Abstract

Abstract Soybean growers widely use the R esistance to H eterodera g lycines 1 ( Rhg1 ) locus to reduce yield losses caused by soybean cyst nematode (SCN). Rhg1 is a tandemly repeated four gene block. Two classes of SCN resistance‐conferring Rhg1 haplotypes are recognized: rhg1‐a (“Peking‐type,” low‐copy number, three or fewer Rhg1 repeats) and rhg1‐b (“PI 88788‐type,” high‐copy number, four or more Rhg1 repeats). The rhg1‐a and rhg1‐b haplotypes encode α‐SNAP (alpha‐ S oluble N SF A ttachment P rotein) variants α‐SNAP Rhg1 LC and α‐SNAP Rhg1 HC, respectively, with differing atypical C‐terminal domains, that contribute to SCN resistance. Here we report that rhg1‐a soybean accessions harbor a copia retrotransposon within their Rhg1 Glyma.18G022500 (α‐SNAP‐encoding) gene. We termed this retrotransposon “ RAC, ” for R hg1 a lpha‐SNAP c opia. Soybean carries multiple RAC ‐like retrotransposon sequences. The Rhg1 RAC insertion is in the Glyma.18G022500 genes of all true rhg1‐a haplotypes we tested and was not detected in any examined rhg1‐b or Rhg1 WT (single‐copy) soybeans. RAC is an intact element residing within intron 1, anti‐sense to the rhg1‐a α‐SNAP open reading frame. RAC has intrinsic promoter activities, but overt impacts of RAC on transgenic α‐SNAP Rhg1 LC mRNA and protein abundance were not detected. From the native rhg1‐a RAC + genomic context, elevated α‐SNAP Rhg1 LC protein abundance was observed in syncytium cells, as was previously observed for α‐SNAP Rhg1 HC (whose rhg1‐b does not carry RAC ). Using a SoySNP50K SNP corresponding with RAC presence, just ~42% of USDA accessions bearing previously identified rhg1‐a SoySNP50K SNP signatures harbor the RAC insertion. Subsequent analysis of several of these putative rhg1‐a accessions lacking RAC revealed that none encoded α‐SNAP Rhg1 LC , and thus, they are not rhg1‐a . rhg1‐a haplotypes are of rising interest, with Rhg4 , for combating SCN populations that exhibit increased virulence against the widely used rhg1‐b resistance. The present study reveals another unexpected structural feature of many Rhg1 loci, and a selectable feature that is predictive of rhg1‐a haplotypes.