Successful intergeneric transfer of a major apple scab resistance gene (Rvi6) from apple to pear and precise comparison of the downstream molecular mechanisms of this resistance in both species.

BACKGROUND: Scab is the most important fungal disease of apple and pear. Apple (Malus x domestica Borkh.) and European pear (Pyrus communis L.) are genetically related but they are hosts of two different fungal species: Venturia inaequalis for apple and V. pyrina for European pear. The apple/V. inaequalis pathosystem is quite well known, whereas knowledge about the pear/V. pyrina pathosystem is still limited. The aim of our study was to analyse the mode of action of a major resistance gene of apple (Rvi6) in transgenic apple and pear plants interacting with the two scab species (V. inaequalis and V. pyrina), in order to determine the degree of functional transferability between the two pathosystems. RESULTS: Transgenic pear clones constitutively expressing the Rvi6 gene from apple were compared to a scab transgenic apple clone carrying the same construct. After inoculation in greenhouse with V. pyrina, strong defense reactions and very limited sporulation were observed on all transgenic pear clones tested. Microscopic observations revealed frequent aborted conidiophores in the Rvi6 transgenic pear / V. pyrina interaction. The macro- and microscopic observations were very comparable to the Rvi6 apple / V. inaequalis interaction. However, this resistance in pear proved variable according to the strain of V. pyrina, and one of the strains tested overcame the resistance of most of the transgenic pear clones. Comparative transcriptomic analyses of apple and pear resistant interactions with V. inaequalis and V. pyrina, respectively, revealed different cascades of molecular mechanisms downstream of the pathogen recognition by Rvi6 in the two species. Signal transduction was triggered in both species with calcium (and G-proteins in pear) and interconnected hormonal signaling (jasmonic acid in pear, auxins in apple and brassinosteroids in both species), without involvement of salicylic acid. This led to the induction of defense responses such as a remodeling of primary and secondary cell wall, lipids biosynthesis (galactolipids in apple and cutin and cuticular waxes in pear), systemic acquired resistance signal generation (in apple) or perception in distal tissues (in pear), and the biosynthesis of phenylpropanoids (flavonoids in apple but also lignin in pear). CONCLUSION: This study is the first example of a successful intergeneric transfer of a resistance gene among Rosaceae, with a resistance gene functioning towards another species of pathogen.

Strain-specific and recessive QTLs involved in the control of partial resistance to Fusarium oxysporum f. sp. melonis race 1.2 in a recombinant inbred line population of melon.

Fusarium oxysporum f. sp. melonis (FOM) causes serious economic losses in melon (Cucumis melo L.). Two dominant resistance genes have been identified, Fom-1 and Fom-2, which provide resistance to races 0 and 2 and races 0 and 1, respectively, however FOM race 1.2 overcomes these resistance genes. A partial resistance to FOM race 1.2 that has been found in some Far East accessions is under polygenic control. A genetic map of melon was constructed to tag FOM race 1.2 resistance with DNA markers on a recombinant inbred line population derived from a cross between resistant (Isabelle) and susceptible (cv. Védrantais) lines. Artificial root inoculations on plantlets of this population using two strains, one that causes wilting (FOM 1.2w) and one that causes yellowing (FOM 1.2y), resulted in phenotypic and genotypic data that enabled the identification of nine quantitative trait loci (QTLs). These QTLs were detected on five linkage groups by composite interval mapping and explained between 41.9% and 66.4% of the total variation. Four digenic epistatic interactions involving seven loci were detected and increased the total phenotypic variation that was explained. Co-localizations between QTLs and resistance gene homologs or resistance genes, such as Fom-2 and Vat, were observed. A strain-specific QTL was detected, and some QTLs appeared to be recessive.

Relationship between Loci conferring downy mildew and powdery mildew resistance in melon assessed by quantitative trait Loci mapping.

ABSTRACT Partial resistance to downy mildew (Pseudoperonospora cubensis) and complete resistance to powdery mildew (Podosphaera xanthii races 1, 2, 3, and 5 and Golovinomyces cichoracearum race 1) were studied using a recombinant inbred line population between 'PI 124112' (resistant to both diseases) and 'Védrantais' (susceptible line). A genetic map of melon was constructed to tag these resistances with DNA markers. Natural and artificial inoculations of Pseudoperonospora cubensis were performed and replicated in several locations. One major quantitative trait loci (QTL), pcXII.1, was consistently detected among the locations and explained between 12 to 38% of the phenotypic variation for Pseudoperonospora cubensis resistance. Eight other Pseudoperonospora cubensis resistance QTL were identified. Artificial inoculations were performed with several strains of four races of Podosphaera xanthii and one race of G. cichoracearum. Two independent major genes, PmV.1 and PmXII.1, were identified and shown to be involved in the simple resistance to powdery mildew. Three digenic epistatic interactions involving four loci were detected for two races of Podosphaera xanthii and one race of G. cichoracearum. Co-localization between PmV.1, resistance genes, and resistance genes homologues was observed. Linkage between the major resistance QTL to Pseudoperonospora cubensis, pcXII.1, and one of the two resistance genes to powdery mildew, PmXII.1, was demonstrated.

Polygenic Inheritance of Partial Resistance to Fusarium oxysporum f. sp. melonis Race 1.2 in Melon.

ABSTRACT Fusarium oxysporum f. sp. melonis is responsible for Fusarium wilt of melon. Race 1.2 strains overcome two dominant resistance genes (Fom-1 and Fom-2) and are further divided into two types depending on the symptoms they cause, yellowing or wilting. Partial resistance to F. oxysporum f. sp. melonis race 1.2 was studied by using a recombinant inbred line (RIL) population that was developed by single seed descent from an F(1) hybrid between 'Isabelle', a partially resistant line, and a susceptible line, 'Védrantais'. Artificial inoculations were performed with a yellowing strain (TST) and a wilting strain (D'Oléon 8) and replicated in six locations. Disease reactions of the parental lines, controls, and RILs were scored using a 1-to-5 scale and by using the area under the disease progress curve (AUDPC). Phenotypic correlations were highly significant between the different locations and experiments. The heritability of the resistance was high, from 0.72 to 0.96, and 4 to 14 genetic factors were estimated to confer resistance to F. oxysporum f. sp. melonis race 1.2. Thirteen other strains were tested with an RILs subset. Some small strainspecific effects may be involved. These results contribute to a better understanding of the polygenic inheritance of the partial resistance to F. oxysporum f. sp. melonis race 1.2.