Powdery mildew caused by the fungus Blumeria graminis f. sp. tritici (Bgt) is a prevalent disease that restricts wheat (Triticum aestivum) production globally. Diverse Bgt resistance genes and alleles are continually needed for wheat disease resistance breeding. We identified a wild emmer wheat (Triticum dicoccoides, WEW) introgression line, R53M, with effective resistance to Bgt isolate E09 starting at the two-leaf stage, during powdery mildew resistance assays in the greenhouse. Genetic analysis indicated that R53M carries a dominant powdery mildew (Pm) resistance gene, designated as PmR53M. We mapped PmR53M to the short arm of chromosome 2B, at the same approximate location as the resistance loci Pm68/MlIW39/PmWR183 from WEW. Sequence analysis revealed that the genetic interval containing the PmR53M locus includes Pm68d, an allelic variant of Pm68. We confirmed the resistance conferred by the PmR53M/Pm68d using virus-induced gene silencing (VIGS) and transgenic assays. This resistance results from the combined effect of two complementary nucleotide-binding and leucine-rich repeat (NLR) genes. In contrast to the all-stage resistance observed with Pm68 and MlIW39, PmR53M only conferred complete resistance to powdery mildew starting at the two-leaf stage, similar to PmWR183, which provides resistance at the three- and four-leaf stages. We developed co-segregating gene-based markers for the identification of PmR53M. The discovery of PmR53M enriches the Pm gene pool in wheat and should facilitate the genetic improvement of powdery mildew resistance.

Powdery mildew (PM), caused by Blumeria graminis f. sp. tritici (Bgt), is one of the destructive wheat diseases worldwide. Wild emmer wheat (Triticum turgidum ssp. dicoccoides, WEW), a tetraploid progenitor of common wheat, is a valuable genetic resource for wheat disease resistance breeding programs. We developed three hexaploid pre-breeding lines with PM resistance genes derived from three WEW accessions. These resistant pre-breeding lines were crossed with susceptible common wheat accessions. Segregations in the F₂ populations were 3 resistant : 1 susceptible, suggesting a single dominant allele in each resistant parent. Mapping of the resistance gene in each line indicated a single locus on the long arm of chromosome 7A, at the approximate location of previously cloned Pm60 from T. urartu. Sanger sequencing revealed three different Pm60 haplotypes (Hap 3, Hap 5, and Hap 6). Co-segregating diagnostic markers were developed for identification and selection of each haplotype. The resistance function of each haplotype was verified by the virus-induced gene silencing (VIGS). Common wheat lines carrying each of these Pm60 haplotypes were resistant to most Bgt isolates and differences in the response arrays suggested allelic variation in response.