The genetics of obligate parthenogenesis in an aphid species and its consequences for the maintenance of alternative reproductive modes.

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.

Durable resistance to stripe rust is due to three specific resistance genes in French bread wheat cultivar Apache.

Quantitative resistance is postulated to be more durable than qualitative (R-gene mediated) resistance, which is usually quickly overcome by the pathogen population. Despite its wide use for nearly 10 years in France, the French bread wheat cultivar Apache remains resistant to stripe rust. Here, we investigated the genetic architecture of cv. Apache resistance to examine whether its durability could be explained by quantitative characteristics. We identified quantitative trait loci (QTL) by composite interval mapping of disease progress data recorded throughout 4 years of field assays. These assays included inoculation with three different pathotypes on a segregating population originating from a cross between cv. Apache and cv. Taldor, a French cultivar susceptible to stripe rust. Three QTLs derived from Apache, QYr.inra-2AS, QYr.inra-2BL and QYr.inra-4B, were detected. Each of these QTLs contributed between approximately 15 and 69 % of the phenotypic variance and corresponds to a race-specific resistance gene. We showed that QYr.inra-2AS and QYr.inra-2BS map to the positions of Yr17 and Yr7, respectively, whereas QYr.inra-4B corresponds to an adult plant resistance gene. Our results demonstrate that a combination of two or more race-specific resistance genes can confer durable resistance provided that it is properly managed at a continental level. Race-specific resistance genes should not be removed from breeding programs provided that they are properly managed.

Characterization of genetic components involved in durable resistance to stripe rust in the bread wheat 'Renan'.

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.

Genetic analysis of durable resistance to yellow rust in bread wheat.

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.

Mapping of quantitative trait loci for field resistance to Fusarium head blight in an European winter wheat.

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.

Study of the relationship between pre-harvest sprouting and grain color by quantitative trait loci analysis in a whitexred grain bread-wheat cross.

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'.

Isolation of a chromosomally engineered durum wheat line carrying the Aegilops ventricosa pchl gene for resistance to eyespot.

The chromosome 7Dv of Aegilops ventricosa (syn. Triticum ventricosum, 2n = 4x = 28, genome DvDvMvMv) carries the gene Pch1 for resistance to eyespot. This gene has previously been transferred to chromosome 7D of bread wheat, T. aestivum (2n = 6x = 42, genome AABBDD). To (1) enhance the level of resistance of bread wheat by increasing the copy number of Pch1, and (2) create eyespot-resistant triticales, meiotically stable Pch1-carrying durum lines were selected from the backcross progenies of a cross between Ae. ventricosa and T. durum cv. Creso ph1c (2n = 4x = 28, genome AABB). The Pch1 transfer, likely resulting from homoeologous recombination, was located at the distal position on the long arm of chromosome 7A. The 7A microsatellite marker Xgwm 698 was found closely linked in repulsion to the introgression in the resistant recombination lines, and the endopeptidase allele located on chromosome 7A of cv. Creso ph1c was lost.

Molecular markers linked to the leaf rust resistance gene Lr24 in different wheat cultivars.

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.