Powdery mildew is one of the major diseases of wheat in regions with a maritime or semi-continental climate which can strongly affect grain yield. The objective of the study was to identify and compare quantitative resistance to powdery mildew of line RE9001 at the adult plant and vernalized seedling stages. RE9001 has no known Pm gene and shows a high level of adult plant resistance in the field. Using 104 recombinant inbred lines (RILs) of an RE9001 · 'Courtot' F8 population, a genetic map was developed with 363 markers distributed over 26 linkage groups and covering 3825 cM. The global map density was 1 locus/10.3 cM. RILs were assessed under field and tunnel greenhouse conditions for 2 years in two locations. Eleven quantitative trait loci (QTL) were detected at the adult stage and they explained 63% of the variation, depending on the environment. Three QTLs were found, at least, in the two environments. One QTL from RE9001, mapped on chromosome 2B, was stable in each environment. This QTL, QPm.inra.2B, explained 10.3-36.6% of the variation and could be mapped in the vicinity of the Pm6 gene. At the vernalized seedling stage, one QTL detected by the isolate 93-27 could be an allele of the Pm3g gene present in 'Courtot'. No residual effect of the Pm3g gene was detected at either stage. Markers flanking the QTL 2B could be useful tools to combine resistance to powdery mildew in wheat cultivars.

The Pm3 resistance locus, located on chromosome 1A in wheat, confers race-specific resistance to the obligate biotrophic fungus Blumeria graminis (DC) E.O. Speer f. sp. tritici, the causal agent of powdery mildew. Several Pm3 alleles are still effective in controlling the disease in Europe. A genetic map was constructed to map the Pm3g allele in the recombinant inbred line progeny from the cross ÔRE9001Õ (susceptible) · ÔCourtotÕ (resistant). Two microsatellite markers were closely mapped to Pm3g. The PSP2999 marker, which cosegregates with this allele, was shown to detect the presence of the Pm3g resistance allele in other cultivars. A collection of 56 wheat cultivars or advanced lines carrying one Pm3 allele was used to assess the allelespecific amplification of the PSP2999 marker. The same amplification pattern was obtained for lines with Pm3a, Pm3b, Pm3e, Pm3f and Pm3g alleles. Twenty genotypes carrying Pm3d showed a specific amplification pattern. This marker allowed the detection of the Pm3d allele in highly resistant lines whose resistance gene combinations were unknown. It was concluded that PSP2999 is a useful marker to detect Pm3 alleles in parents and to manage them in breeding programmes.

Race-specific resistance genes to powdery mildew have been extensively used in wheat breeding programs, but the complete resistance they provide breaks down when confronted by pathogen isolates with matching virulence. However, when overcome, some race-specific genes have a residual action leading to a reduction of the symptoms. Our objective was to determine if the resistance genes MlRE and Pm4b have a residual effect on adult plant resistance (APR) and on vernalized seedling plant resistance (VPR) in the line RE714. Individuals from two populations (double haploid [DH] and F(3) families) were genotyped for the race-specific genes MlRE and Pm4b and assessed for their resistance under field conditions at the adult plant stage (in 1996 and 1997 for the DH lines and in 1997 for the F(3) families). Vernalized seedlings of the DH population were tested with four powdery mildew isolates. Only the MlRE gene had a significant effect (dominant type) on APR. Neither MlRE nor Pm4b had a significant effect on VPR. The dominant residual effect of the defeated race-specific gene MlRE was a component of APR in the line RE714.

Powdery mildew (Blumeria graminis f. sp. tritici) is one of the major diseases of wheat (Triticum aestivum). Adult plant resistance (APR) to powdery mildew is considered more durable than resistance conferred by major race-specific resistance genes. The objective of the present study was a better understanding of the genetic basis of APR in RE714 by means of QTL analysis of several resistance scores along the growing season. A population of 160 recombinant inbred lines obtained from the cross between RE714 and Hardi (susceptible) was assessed for APR under natural infection conditions during 3 years and a genetic map with whole genome coverage was developed with microsatellite and AFLP markers in this population. Two major QTL on chromosomes 5D and 6A were detected each year, and 6 minor QTL were detected only in 1 or 2 years. The QTL on chromosome 5D was detected during all the growing season each year and its R 2 value varied between 8.5 and 56.3%, whereas the QTL on chromosome 6A was detected at 1-4 scoring dates in the 3 years, and its R 2 value varied between 6.1 and 20.5%. The two QTL explained between 24.4 and 52.1% of the phenotypic variance for AUDPC, depending on the year. The models including QTL and cofactors in the composite interval mapping explained between 29 and 72% of the variance. The molecular markers linked to the two major QTL could be used in marker-assisted selection for adult plant resistance to powdery mildew.

Powdery mildew (Blumeria graminis f. sp. tritici) is one of the major diseases of wheat (Triticum aestivum). The objective of the present study was to describe the quantitative resistance to powdery mildew of the winter wheat line RE714 at the seedling stage and to identify microsatellite markers tightly linked to the RE714 resistance QTL, which could be used in marker-assisted selection. A population of 160 recombinant inbred lines obtained from the cross between RE714 (resistant) and Hardi (susceptible) was genotyped with microsatellite and AFLP markers. Fifteen powdery mildew isolates were used to test the resistance of these lines at the seedling stage. QTL analysis enabled us to identify three major QTLs controlling powdery mildew resistance in RE714: a QTL located on chromosome 2A, corresponding to the Pm4b gene, explaining 76–93% of the phenotypic variance for resistance to six isolates; two QTLs located on chromosomes 5D and 6A, each explaining 20–67% of the phenotypic variance for resistance to five isolates. A minor QTL for resistance to four of the six isolates revealing Pm4b was detected in the same region as the 5D QTL. Other minor QTLs were detected on chromosomes 2A and 6B, explaining, respectively, 10.9 and 11.5% of the phenotypic variance for resistance to isolate 96-27. The maps around the three major QTLs were enriched with microsatellite markers that could be used in marker-assisted selection of these QTLs.