Genome-wide associations within diverse wild apple germplasm for postharvest blue mold resistance to Penicillium expansum

Post-harvest disease caused by the blue mold fungus, Penicillium expansum, accounts for a substantial proportion of economic losses in the United States apple industry. Multiple modes of entry in the apple supply chain, plus emerging fungicide resistance, limit the current and long-term viability of using chemical controls alone. Previous phenotypic screens of Malus accessions in the USDA-ARS apple germplasm have identified varying levels of blue mold disease resistance in some wild apple accessions and hybrids. These wild apple species contain reservoirs of genetic resistance that can be integrated into apple breeding programs to complement the previously identified qM-Pe3.1 marker from M. sieversii. We sought to identify these novel loci by combining historical phenotypes of the USDA-ARS wild apple germplasm with low-pass genomic sequencing to perform association mapping. Multi-locus mixed models identified five single nucleotide polymorphisms (SNPs) significantly associated with reduction of post-harvest rot under high concentration of P. expansum inoculum, and one SNP associated under low inoculum concentration. Within a 25,000 base pair window of these SNPs, we found candidate genes encoding proteins with known pathogen immune response and defense roles, such as a Cobra-like 7, flavin monooxygenase, LRR receptors, PR5-like receptor kinase, and a putative resistance protein RGA3. We present these loci as targets for identifying accessions with beneficial alleles that can be targeted for fine mapping and used in Malus breeding programs to achieve M. domestica lines with natural post-harvest rot resistance.