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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 #338596
Title: Transcriptomic response of resistant (P161983-Malus sieversii) and susceptible ("Royal Gala") genotypes of apple to blue mold (penicillium expansum) infection

Author
item BALLESTER, ANA-ROSA - Instituto De Agroquimica Y Technologia De Alimentos
item Norelli, John
item Burchard, Erik
item ABDELFATTAH, AHMED - University Of Reggio Calabria
item LEVIN, ELENA - Volcani Center (ARO)
item GONZALEZ-CANDELAS, LUIS - Instituto De Agroquimica Y Technologia De Alimentos
item DROBY, SAMIR - Volcani Center (ARO)
item Wisniewski, Michael

Submitted to: Frontiers in Plant Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/2/2017
Publication Date: 11/16/2017
Citation: Ballester, A., Norelli, J.L., Burchard, E.A., Abdelfattah, A., Levin, E., Gonzalez-Candelas, L., Droby, S., Wisniewski, M.E. 2017. Transcriptomic response of resistant (P161983-Malus sieversii) and susceptible ("Royal Gala") genotypes of apple to blue mold (penicillium expansum) infection. Frontiers in Plant Science. 8(1981):1-16.

Interpretive Summary: Blue mold, a postharvest pathogen (Penicillium expansum) of apple and other fruits, is a major source of fruit losses to growers and consumers. The main approach for managing blue mold during apple processing and storage is the use of chemical fungicides. There is a growing need to develop alternative strategies for managing blue mold due to a build-up of resistance to the chemical fungicides, and consumer demand for pesticide-free produce. The development of disease resistant germplasm is one alternative that would eliminate the need for the use of postharvest fungicides, however, this approach has not been used in the breeding of new apple varieties for a number of reasons, among which is the lack of blue mold resistance in any of the commercial apple varieties. Malus sieversii, a progenitor of the modern apple is considered to be a reservoir for many economical traits, including disease resistance. Over the past several years, USDA-ARS scientists at Kearneysville, WV have developed genetic markers for blue mold resistance derived from an elite selection of M. sieversii that can be used by breeders to incorporate blue mold resistance into their breeding program. The current study was conducted to better understand the molecular basis for resistance in M. sieversii – PI613981. Results indicated that the fruit from the resistant genotype (M. sieversii – PI613981) underwent a faster response to both wounding and wounding following by inoculation with the blue mold fungus, than fruit from the susceptible, ‘Royal Gala’ genotype. Seven of the differentially expressed genes were located in the same region of chromosome 3 where the resistance markers were identified. This information will be used to examine the sequence of these genes in the resistant and susceptible genotypes in order to determine the genetic basis for blue mold resistance.

Technical Abstract: Malus sieversii from Central Asia is a progenitor of the modern domesticated apple (Malus × domestica). Several accessions of M. sieversii are highly resistant to the postharvest pathogen Penicillium expansum. A previous study identified the qM-Pe3.1 QTL on LG3 for resistance to P. expansum in the mapping population GMAL4593, developed using the resistant accession, M. sieversii -PI613981, and the susceptible cultivar ‘Royal Gala’ (M. domestica), as parents. The goal of the present study was to characterize the transcriptomic response of susceptible ‘Royal Gala’ and resistant PI613981 apple fruit to wounding and inoculation with P. expansum using RNA-Seq. Transcriptomic analyses 0 to 48 h post inoculation suggest a stronger and quicker response to wounding and wounding plus inoculation with P. expansum in PI613981 than in ’Royal Gala’. The rapidity and the continuity of the wound response suggests that the resistant genotype (Malus sieversii - PI613981) may recognize the presence of effector molecules secreted by the necrotrophic pathogen, P. expansum, or block host response that would trigger cell death and thus increase the availability of nutrients that could be utilized by the pathogen for infection and decay development. At least seven DEGs were mapped to the qM-Pe3.1 QTL (M×d v.1: 26,848,396 – 28,424,055) on LG3, and represent potential candidate genes responsible for the observed resistance QTL in M. sieversii – PI613981.