In many wheat ( Triticum aestivumL.) growing areas, pre-harvest sprouting (PHS) may cause important damage, and in particular, it has deleterious effects on bread-making quality. The relationship between PHS and grain color is well known and could be due either to the pleiotropic effect of genes controlling red-testa pigmentation ( R) or to linkage between these genes and other genes affecting PHS. In the present work, we have studied a population of 194 recombinant inbred lines from the cross between two cultivars, 'Renan' and 'Récital', in order to detect QTLs for both PHS resistance and grain color. The variety 'Renan' has red kernels and is resistant to PHS, while 'Récital' has white grain and is highly susceptible to PHS. A molecular-marker linkage map of this cross was constructed using SSRs, RFLPs and AFLPs. The population was evaluated over 2 years at Clermont-Ferrand (France). PHS was evaluated on mature spikes under controlled conditions and red-grain color was measured using a chromameter. Over the 2 years, we detected four QTLs for PHS, all of them being co-localized with QTLs for grain color. Three of them were located on the long arm of chromosomes 3 A, 3B and 3D, close to the loci where the genes R and taVp1 were previously mapped. For these three QTLs, the resistance to PHS is due to the allele of the variety 'Renan'. Another co-located QTL for PHS and grain color was detected on the short arm of chromosome 5 A. The resistance for PHS for this QTL is due to the allele of 'Récital'.

Fusarium head blight (FHB) caused by Fusarium culmorum is an economically important disease of wheat that may cause serious yield and quality losses under favorable climate conditions. The development of disease-resistant cultivars is the most effective control strategy. Worldwide, there is heavy reliance on the resistance pool originating from Asian wheats, but excellent field resistance has also been observed among European winter wheats. The objective of this study was to map and characterize quantitative traits loci (QTL) of resistance to FHB among European winter wheats. A population of 194 recombinant inbred lines (RILs) was genotyped from a cross between two winter wheats Renan (resistant)/Récital (susceptible) with microsatellites, AFLP and RFLP markers. RILs were assessed under field conditions For 3 years in one location. Nine QTLs were detected, and together they explained 30-45% of the variance, depending on the year. Three of the QTLs were stable over the 3 years. One stable QTL, QFhs.inra.2b, was mapped to chromosome 2B and two QTLs QFhs.inra.5a2 and QFhs.inra5a3, to chromosome 5A; each of these QTLs explained 6.9-18.6% of the variance. Other QTLs were identified on chromosome 2A, 3A, 3B, 5D, and 6D, but these had a smaller effect on FHB resistance. One of the two QTLs on chromosome 5A was linked to gene B1 controlling the presence of awns. Overlapping QTLs for FHB resistance were those for plant height or/and flowering time. Our results confirm that wheat chromosomes 2A, 3A, 3B, and 5A carry FHB resistance genes, and new resistance factors were identified on chromosome arms 2BS and 5AL. Markers flanking these QTLs should be useful tools for combining the resistance to FHB of Asian and European wheats to increase the resistance level of cultivars.

Stripe rust, caused by Puccinia striiformis f. tritici, is one of the most widespread and destructive wheat diseases in areas where cool temperatures prevail. The wheat cv. Renan, carrying the specific gene Yr17, has shown effective resistance for a long time, even though some pathotypes overcame the Yr17 gene. The objectives of this study were to locate and map genetic loci associated with adult-plant resistance (APR) to stripe rust in a recombinant inbred line population derived from a cross between Renan (resistant) and Récital (susceptible). Field assays were performed for 4 years (1995, 1996, 2005, and 2006) to score disease-progress data and identify APR quantitative trait loci (QTLs). Three QTLs, QYr.inra-2BS, QYr.inra-3BS, and QYr.inra-6B, with resistance alleles derived from Renan were detected in 1995 to 1996 with the 237E141 pathotype, which is avirulent against genotypes carrying Yr17. These QTLs were stable and explained a major part of the phenotypic variation seen in 2005 to 2006, when the 237E141 V17 pathotype was used. Each of these QTLs contributed approximately 4 to 15% of the phenotypic variance and was effective at different adult plant stages. Interactions were observed between some markers of the Yr17 gene and three Renan QTLs: QYr.inra-2BS, QYr.inra-3BS, and QYr.inra-6B. Resistance based on the combination of different APR types should provide durable resistance to P. striiformis.

Yellow rust, caused by Puccinia striiformis, is one of the most damaging diseases affecting bread wheat in temperate regions. Although resistance to yellow rust is frequently overcome by new virulent races, a durable form of resistance in the French bread wheat Camp Remy (CR) has remained effective since its introduction in 1980. We used 217 F7 recombinant inbred lines (RILs) derived from the cross between CR and the susceptible cultivar Recital to identify and map quantitative trait loci (QTLs) involved in durable yellow rust resistance. Six significant QTLs that were stable over a 4-year period were detected. Two QTLs, denoted QYr.inra-2DS and QYr.inra-5BL.2, were located on the short arm of chromosome 2D and the long arm of chromosome 5B, respectively. Each explained on average 25-35% of the observed phenotypic variation and were probably inherited from Cappelle Desprez, a parent of CR that confers durable adult plant resistance to yellow rust. QYr.inra-2DS probably corresponds to the Yr16 gene. The most consistent QTL, designated QYr.inra-2BL, was located on the centromeric region of chromosome 2B and explained 61% of the phenotypic variation in 2003. This QTL was responsible for seedling-stage resistance and may correspond to a cluster of genes, including Yr7. The remaining QTLs were mapped to the short arm of chromosome 2B (R2=22-70%) and to the long arm of chromosomes 2A (R2=0.20-0.40) and 5B (R2=0.18-0.26). This specific combination of seedling and adult plant resistance genes found in CR and CD may constitute the key to their durable resistance against yellow rust.

Resistance to Puccinia striiformis was examined in nine wheat recombinant inbred lines (RILs) from a cross between 'Camp Rémy' (resistant parent) and 'Récital' (susceptible parent) using an isolate of a strain common to the northwestern European population before 2011 (old) and two additional isolates, one representing an aggressive and high-temperature-adapted strain (PstS2) and another representing a virulence phenotype new to Europe since 2011 (new). The RILs carried different combinations of quantitative trait loci (QTL) for resistance to P. striiformis. Under greenhouse conditions, the three isolates gave highly contrasting results for infection type, latent period, lesion length, and diseased leaf area. The PstS2 isolate revealed Yr genes and QTL which conferred complete resistance in adult plants. Six QTL had additive effects against the old isolate whereas the effects of these QTL were significantly lower for the new isolate. Furthermore, the new isolate revealed previously undetected resistance in the susceptible parent. Disease severity under field conditions agreed with greenhouse results, except for Camp Rémy being fully resistant to the new isolate and for two RILs being susceptible in the field. These results stress the need of maintaining high genetic diversity for disease resistance in wheat and of using pathogen isolates of diverse origin in studies of host resistance genetics.

Although loss of sex is widespread among metazoans, the genetic mechanisms underlying the transition to asexuality are poorly understood. Aphids are good models to address this issue because they frequently show reproductive-mode variation at the species level, involving cyclical parthenogens (CP) that reproduce sexually once a year and obligate parthenogens (OP) that reproduce asexually all year round. Here, we explore the genetic basis of OP in the cereal aphid Sitobion avenae by crossing several genotypes with contrasting reproductive modes and then characterising the reproductive phenotypes of F1 and F2 offspring. The analysis of phenotypic variation in F1 and F2 progenies suggests that at least two autosomal loci control OP in S. avenae. First, the transition to asexuality seems to depend on a single recessive locus, because the offspring from self-crossed cyclical parthenogenetic genotypes contain either 0 or 25% OP. Second, as we observed OP in the F1 progenies from crosses between CP and OP, and some CP in the offspring from outcrossed OP, a dominant 'suppressor' gene may also be involved, being inactive when in a recessive homozygous state in CP; this is the most parsimonious explanation for these results. This oligogenic inheritance of OP in S. avenae appears to be an efficient genetic system to generate new OP genotypes continually. It also allows asexuality-inducing alleles to be protected locally during harsh winters when extreme frost kills most OP, and then to spread very quickly after winter.

The aim of this study was to find molecular markers (RAPD and SCAR) for the wheat leaf rust resistance gene Lr24. A backcross line, RL 6064, possessing a single resistance gene to leaf rust (Lr24) and its recurrent parent 'Thatcher' were used to find RAPD markers linked to the Lr24 gene. Among 125 RAPD primers tested, only one (OP-H5) detected an additional band in the resistant line RL 6064. The genetic linkage of this molecular marker to Lr24 was tested on a segregating F2 population derived from a cross between the leaf rust resistant line RL 6064 and the susceptible line 'Chinese Spring'. This marker showed complete linkage to the Lr24 resistance gene. A more reliable and specific marker for this resistance gene was made by converting it into a sequence characterized amplified region (SCAR). The presence of a single amplification product allowed direct detection of the gene in the test tube by the addition of ethidium bromide. This SCAR marker linked to the leaf rust resistance gene Lr24 could be used easily in a practical breeding program.

Unlike qualitative plant resistance, which confers immunity to disease, quantitative resistance confers only a reduction in disease severity and this can be nonspecific. Consequently, the outcome of its deployment in cultivar mixtures is not easy to predict, as on the one hand it may reduce the heterogeneity of the mixture, but on the other it may induce competition between nonspecialized strains of the pathogen. To clarify the principles for the successful use of quantitative plant resistance in disease management, we built a parsimonious model describing the dynamics of competing pathogen strains spreading through a mixture of cultivars carrying nonspecific quantitative resistance. Using the parameterized model for a wheat-yellow rust system, we demonstrate that a more effective use of quantitative resistance in mixtures involves reinforcing the effect of the highly resistant cultivars rather than replacing them. We highlight the fact that the judicious deployment of the quantitative resistance in two- or three-component mixtures makes it possible to reduce disease severity using only small proportions of the highly resistant cultivar. Our results provide insights into the effects on pathogen dynamics of deploying quantitative plant resistance, and can provide guidance for choosing appropriate associations of cultivars and optimizing diversification strategies.