Wound responses of wild apples suggest multiple resistance mechanism against blue mold decay

Abstract

Blue mold caused primarily by Penicillium expansum and to a lesser extent other Penicillium spp. is the most destructive disease of stored apples in the US and worldwide. It was recently shown that resistance to blue mold exists in wild apple germplasms, Malus sieversii, from Kazakhstan and in other species from different regions maintained as a collection in Geneva, NY. We initiated studies to determine the durability and the mechanism(s) of resistance to P. expansum in select wild apple accessions. Wound responses (up to 96h in 24h intervals), affecting P. expansum infection, and related cytological changes were determined in accessions with varying levels of resistance. In general, the more resistant the accession, the quicker the wound response that prevented the fungus from infecting tissue and causing decay. No decay developed on immune apple accessions, even when inoculated immediately after wounding at the inoculum concentration of 105 conidia/mL. On a moderately resistant accession, a 24h interval between wounding and inoculation was sufficient to avert decay. Reactive oxygen species (ROS) were detected at high levels immediately after wounding in the immune as well as susceptible accessions. Callose and lignin/suberin appears to play a minor role in resistance responses. Our results indicate the presence of a high level of durable resistance/immunity in the wild apples which is governed by several mechanism(s). This presents a new challenge for explaining the observed resistance and at the same time creates an opportunity for exploiting these resistant mechanisms in breeding programs to incorporate resistance to fruit decays into commercial cultivars.