Sustainable deployment of QTLs conferring quantitative resistance to crops: first lessons from a stochastic model

Quantitative plant disease resistance is believed to be more durable than qualitative resistance, since it exerts less selective pressure on the pathogens. However, the process of progressive pathogen adaptation to quantitative resistance is poorly understood, which makes it difficult to predict its durability or to derive principles for its sustainable deployment. Here, we study the dynamics of pathogen adaptation in response to quantitative plant resistance affecting pathogen reproduction rate and its carrying capacity. We developed a stochastic model for the continuous evolution of a pathogen population within a quantitatively resistant host. We assumed that pathogen can adapt to a host by the progressive restoration of reproduction rate or of carrying capacity, or of both. Our model suggests that a combination of QTLs affecting distinct pathogen traits was more durable if the evolution of repressed traits was antagonistic. Otherwise, quantitative resistance that depressed only pathogen reproduction was more durable. In order to decelerate the progressive pathogen adaptation, QTLs that decrease the pathogen's ability to extend must be combined with QTLs that decrease the spore production per lesion or the infection efficiency or that increase the latent period. Our theoretical framework can help breeders to develop principles for sustainable deployment of quantitative trait loci.

Construction of an integrated consensus map of the Apple genome based on four mapping populations

An integrated consensus genetic map for apple was constructed on the basis of segregation data from four genetically connected crosses (C1¿=¿Discovery × TN10-8, C2¿=¿Fiesta × Discovery, C3¿=¿Discovery × Prima, C4¿=¿Durello di Forli × Fiesta) with a total of 676 individuals using CarthaGene® software. First, integrated female¿male maps were built for each population using common female¿male simple sequence repeat markers (SSRs). Then, common SSRs over populations were used for the consensus map integration. The integrated consensus map consists of 1,046 markers, of which 159 are SSR markers, distributed over 17 linkage groups reflecting the basic chromosome number of apple. The total length of the integrated consensus map was 1,032 cM with a mean distance between adjacent loci of 1.1 cM. Markers were proportionally distributed over the 17 linkage groups (¿ 2¿=¿16.53, df¿=¿16, p¿=¿0.41). A non-uniform marker distribution was observed within all of the linkage groups (LGs). Clustering of markers at the same position (within a 1-cM window) was observed throughout LGs and consisted predominantly of only two to three linked markers. The four integrated female¿male maps showed a very good colinearity in marker order for their common markers, except for only two (CH01h01, CH05g03) and three (CH05a02z, NZ02b01, Lap-1) markers on LG17 and LG15, respectively. This integrated consensus map provides a framework for performing quantitative trait locus (QTL) detection in a multi-population design and evaluating the genetic background effect on QTL expression

Aggressiveness of eight Venturia inaequalis isolates virulent or avirulent to the major resistance gene Rvi6 on a non-Rvi6 apple cultivar

For sustainable management of scab-resistant apple cultivars, it is necessary to understand the role of aggressiveness in the adaptation of Venturia inaequalis populations and particularly the costs to the organism of acquiring additional virulence. The aims of the present study were (i) to identify the quantitative variables that are most important in determining the differences in aggressiveness among groups of V. inaequalis isolates, and (ii) to ascertain whether virulent and avirulent isolates of V. inaequalis differ significantly in aggressiveness. The aggressiveness of eight isolates that differed in their virulence to the major resistance gene Rvi6 was compared on the non-Rvi6 apple cv. Gala. Three components of aggressiveness, namely lesion density, the number of spores per square centimetre of leaf area, and the number of spores per lesion, were evaluated 21 days after inoculation, and the kinetics of lesion density over time were analysed in terms of maximum lesion density, length of latent period and rate of lesion appearance. On the second youngest but fully developed leaf at the time of inoculation, maximum lesion density in the virulent group was 20% lower and the latent period 7% longer, than in the avirulent group. However, the alternative hypothesis, namely that isolates had adapted to quantitative resistance present in cv. Gala depending on their cultivar of origin, could not be rejected. The analysis of the kinetics of lesion density by a non-linear mixed-effect model proved useful in the assessment of aggressiveness

Inheritance studies of apple scab resistance and identification of Rvi14, a new major gene that acts together with other broad-spectrum QTL

Scab, caused by the fungal pathogen Venturia inaequalis, is the most common disease of cultivated apple (Malus domestica). The fungal races 6 and 7 have now overcome the major resistance gene Vf, which is widely used in apple breeding programmes. New breeding strategies to achieve durable resistance are thus necessary. The aim of this study was to determine the genetic basis of quantitative resistance of the apple cultivar ‘Du¨lmener Rosenapfel’, known to be scab resistant under different environmental conditions. An F1 progeny derived from the cross between the susceptible cultivar ‘Gala’ and ‘Du¨lmener Rosenapfel’ was tested in a greenhouse with a multi-isolate inoculum of V. inaequalis. Rvi14, a new major gene that conditions a chlorotic-type reaction, was mapped on linkage group (LG) 6 in a genomic region not known to be involved in disease resistance. A further three quantitative trait loci (QTL) for resistance were identified. One co-localized with Rvi14 on LG6, whereas the remaining two were detected on LG11 and LG17, in genomic regions already reported to carry broad-spectrum QTL in other genetic backgrounds. Since a selective genotyping approach was used to detect QTL, an expectation-maximization (EM) computation was used to estimate the corrected QTL contributions to phenotypic variation and was validated by entire progeny genotyping

A new pear scab resistance gene Rvp1 from the European pear cultivar ‘Navara’ maps in a genomic region syntenic to an apple scab resistance gene cluster on linkage group 2

Scab, caused by the ascomycete fungus Venturia pirina, leads to severe damage on European pear varieties resulting in a loss of commercial value and requiring frequent use of fungicides. Identifying scab resistance genes, developing molecular markers linked to these genes and establishing marker-assisted selection would be an effective way to improve European pear breeding for scab resistance. Most of the European pear cultivars (Pyrus communis) are currently reported to be sensitive. The pear cultivar ‘Navara’ was shown to carry a major scab resistance gene whose phenotypic expression in seedling progenies was a typical stellate necrosis symptom. The resistance gene was called Rvp1, for resistance to V. pirina, and was mapped on linkage group 2 of the pear genome close to microsatellite marker CH02b10. This genomic region is known to carry a cluster of scab resistance genes in apple indicating a first functional synteny for scab resistance between apple and pear