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ARS Home » Northeast Area » Kearneysville, West Virginia » Appalachian Fruit Research Laboratory » Innovative Fruit Production, Improvement, and Protection » Research » Publications at this Location » Publication #335858
Title: Genotyping-by-sequencing markers facilitate the identification of quantitative trait loci controlling resistance to Penicillium expansum in Malus sieversii

Author
item Norelli, John
item Wisniewski, Michael
item Fazio, Gennaro
item Burchard, Erik
item Gutierrez, Benjamin
item LEVIN, ELENA - Volcani Center (ARO)
item DROBY, SAMIR - Volcani Center (ARO)

Submitted to: PLOS ONE
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/13/2017
Publication Date: 3/3/2017
Citation: Norelli, J.L., Wisniewski, M.E., Fazio, G., Burchard, E.A., Gutierrez, B.L., Levin, E., Droby, S. 2017. Genotyping-by-sequencing markers facilitate the identification of quantitative trait loci controlling resistance to Penicillium expansum in Malus sieversii. PLoS One. doi: 10.1371/journal.pone.0172949.

Interpretive Summary: Blue mold is the most important postharvest disease of apple worldwide and results in significant financial losses. There are no defined sources of resistance to blue mold in domesticated apple; however, resistance has been described in wild apple accessions including plant introduction (PI) 613981. The purpose of this study was to identify the genetic loci controlling resistance to blue mold in PI613981. A family of 169 individuals resulting from a cross of between the domesticated Gala apple and wild apple PI613981 was evaluated for blue mold resistance, genotyped to develop a genetic linkage map, and then analyzed for the presence of genetic loci associated with resistance. A genetic linkage map was developed using conventional genetic markers called SSRs and SNPs, and a second map was developed that used both of these conventional markers and a new type of GBS marker that result from next generation DNA sequencing of the individuals in the family. A genetic locus that had a large effect on blue mold resistance was identified on chromosome 3 of PI613981. Another genetic locus on chromosome 10 of the domesticated Gala apple parent also had a minor effect on blue mold resistance. When the genetic analysis was conducted using the map composed of only conventional SSR and SNP markers, the minor effect locus from Gala apple was detected, but the major effect locus from PI613981 was not detected due to poor coverage of the region of the genome containing the resistance locus. Subsequent addition of GBS markers to the map provided better marker coverage and facilitated the identification of the genetic factor in PI613981 controlling high levels of resistance. DNA tests for the blue mold resistance characterized in this study will be used in apple breeding programs to identify apple seedlings resistant to blue mold. The availability of new high quality apple cultivars with resistance to blue mold will enhance the economic viability of the apple industry by reducing production costs and losses, as well as reduce the human health risks associated with pesticide use and toxin (patulin) production by the blue mold fungus.

Technical Abstract: Blue mold caused by Penicillium expansum is the most important postharvest disease of apple worldwide and results in significant financial losses. There are no defined sources of resistance to blue mold in domesticated apple; however, resistance has been described in wild Malus sieversii accessions including plant introduction (PI) 613981. The objective of the present study was to identify the genetic loci controlling resistance to blue mold in PI613981. We describe the first quantitative trait loci (QTL) reported in the Rosaceae subfamily Maloideae conditioning resistance to Penicillium expansum on genetic linkage group 3 (qM-Pe3.1) and linkage group 10 (qM-Pe10.1). These loci were identified in a Malus x domestica ‘Royal Gala’ x M. sieversii PI613981 family (GMAL4593) based on blue mold lesion diameter (7 days post-inoculation) in mature, wounded apple fruit inoculated with P. expansum. Phenotypic analyses were conducted in 169 progeny over a four-year-period. PI613981 was the source of qM-Pe3.1, a QTL with a major effect on blue mold resistance, accounting for 27.5% of the experimental variability. It mapped from 67.3 to 74 cM on linkage group 3 of the GMAL4593 genetic linkage map. qM-Pe10.1 mapped from 73.6 to 81.8 cM on linkage group 10. It had less of an effect on resistance, accounting for 14% of the experimental variation, and ‘Royal Gala’ was the primary contributor to the resistance effect of this QTL. Both parents, however, appeared to contribute to the least square mean blue mold lesion diameter in an additive manner at qM-Pe10.1. A GMAL4593 genetic linkage map composed of simple sequence repeats, and ‘Golden Delicious’ single nucleotide polymorphism markers were able to detect qM-Pe10.1 but failed to detect qM-Pe3.1. The subsequent addition of genotyping-by-sequencing markers to the linkage map provided better coverage of the PI613981 genome on linkage group 3 and facilitated discovery of qM-Pe3.1.