Open AccessGenetics of Host-Pathogen Relationships Between Venturia inaequalis Races 6 and 7 and Malus Species
Author(s) -
G. Bénaouf,
Luciana Parisi
Publication year - 2000
Publication title -
phytopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.264
H-Index - 131
eISSN - 1943-7684
pISSN - 0031-949X
DOI - 10.1094/phyto.2000.90.3.236
Subject(s) - venturia inaequalis , biology , malus , apple scab , gene , genetics , clone (java method) , virulence , pathogen , strain (injury) , cultivar , hypersensitive response , r gene , host (biology) , genotype , plant disease resistance , botany , anatomy , fungicide
Resistance to scab originating from Malus floribunda clone 821 is the most widely form of resistance used in apple breeding programs. A dominant gene, named Vf, was introgressed from this clone into recent cultivars, although the genetic determinants of the resistance of M. floribunda 821 are apparently more complex than a single gene. The appearance of new races overcoming the resistance of cultivars with the Vf gene, the parental clone, or both made it possible to undertake a genetic analysis of host-pathogen interactions. The segregation of resistance in progenies of crosses from ‘Golden Delicious’ × M. floribunda 821 and ‘Golden Delicious’ × ‘Idared’ into five strains of Venturia inaequalis—races 1 (strains 104, 1093, and 301), 6 (strain 302), and 7 (strain 1066)—demonstrated the existence of a second dominant gene in M. floribunda 821. This gene, independent of Vf, was named Vfh because it seemed to induce a hypersensitive reaction. The results obtained with strain 1066, virulent to M. floribunda 821, allowed identification of another dominant gene, Vg, responsible for the resistance of ‘Golden Delicious’ to this strain. Vg is also carried by ‘Florina’, which was selected for its Vf resistance. The pathogenicity of a progeny originating from a cross between V. inaequalis strains 1066 and 301, characterized in vitro on leaf disks of differential genotypes, revealed two independent avirulence genes involved in the pathogenicity toward the Vg and Vf genes, respectively. These avirulence genes were named Avr Vg and Avr Vf. The host-pathogen interactions detected are consistent with a gene-for-gene relationship.