vfett@mail.ubc.ca; samuel.holden@ubc.ca; curtis.pozniak@usask.ca; gurcharn.brar@ualberta.ca

Wheat stripe rust is among the five priority one wheat diseases in Canada. Each infection cycle produces trillions of Puccinia striiformis f. sp. tritici (Pst) spores, which accumulate mutations that threaten to evade host recognition and overcome disease resistance. Resistance bred into new cultivars is often defeated within a few years under high disease pressure. For this reason, novel sources of stripe rust resistance are needed to limit yield losses, which can reach 60% in epidemic years. Bread wheat relatives, like spelt wheat, are reservoirs of resistance genes that can be mined for improving elite cultivars.

Two spelt wheat lines, ‘CDC Silex’ and ‘10Spelt17’, have shown non-race-specific near immunity at the adult plant stage over multiple field seasons in British Columbia and in Saskatchewan, and against all tested Pst races in controlled environment growth chambers. Both cultivars showed susceptibility to all tested Pst races at the seedling stage, indicating that the resistance is only expressed at the adult plant stage.

The adult plant resistance in the spelt wheat lines is novel as no adult plant resistance (APR) gene has been identified in spelt and the resistance phenotype confers near immune response unlike all known APRs in wheat. Through allelism test, we proved that both the spelt wheat lines carry same resistance gene. When the spelt wheat lines were crossed with ‘Avocet’ (a susceptible bread wheat), the resulting F2 and F2:3 populations from each resistant spelt did not show expected Mendelian segregation ratios for stripe rust resistance. We observed severe segregation distortion to the susceptible phenotype.

Interestingly, when crossed with various CWRS (Canada Western Red Spring) elite cultivars, both resistant spelt lines generated susceptible F1 progeny, however, the F1 from ‘CDC Silex’ and ‘CDC Origin’ (susceptible spelt wheat) were stripe rust resistant.

To map the resistance loci in ‘CDC Silex’ and to develop DNA markers associated with the resistance, we performed BSAseq on a bi-parental F2 population of ‘CDC Silex’ and ‘CDC Origin’. We have generated a high-quality genome assembly of ‘CDC Silex’ which was used to anchor polymorphic SNPs between resistant and susceptible F2 bulks and develop KASP markers linked to the genomic region conferring resistance.

We identified a region on 2D chromosome that controls the resistance phenotype. By developing KASP assays, we have fine-mapped the region. Additionally, by looking at haplotype of the locus in spelt/bread wheat RILs, we have attempted to identify susceptibility factor/suppressor of resistance.