Blackleg, caused by Leptosphaeria maculans (Desm.) Ces. et de Not., is a major disease of oilseed rape (Brassica napus L.) worldwide. Molecular markers would be useful tools to assist breeding for blackleg resistance. The objective of this study was (i) to map and characterize quantitative trait loci (QTL) for field blackleg resistance in doubled haploid (DH) and F2:3 populations from the cross ‘Darmor’ (resistant) × ‘Samourai’ (susceptible) and (ii) to compare QTL with those previously identified in the cross ‘Darmor‐bzh’ × ‘Yudal’. A total of 134 DH lines and 185 F2:3 families were genotyped with random amplified polymorphic DNA (RAPD) and restriction fragment length polymorphism (RFLP) markers and assessed for a disease index of resistance in 1998 and/or 1999 in one location. Genetic maps derived from the two populations included a total of 257 and 81 markers, respectively. Up to 30% of these markers were common to the Darmor‐bzh × Yudal map previously used. A total of six and four genomic regions were associated with resistance in the DH and F2:3 populations, respectively. They collectively explained 36 to 42% of the variation within each year and population. Three of them were consistent across the two populations derived from Darmor × Samourai cross and expressed dominant or overdominant effects. Four favorable alleles were derived from the susceptible parent. A total of 16 genomic regions were revealed for blackleg resistance in the two crosses Darmor‐bzh × Yudal and Darmor × Samourai studied. Four of them were consistent over the two crosses. The inconsistencies observed between populations and crosses can be explained by different genetic backgrounds and disease infestation levels. For marker‐assisted selection, these results suggest that QTL mapping must be carried out separately for each population.

In allopolyploid species, fair meiosis could be challenged by homeologous chromosome pairing and is usually achieved by the action of homeologous pairing suppressor genes. Oilseed rape (Brassica napus) haploids (AC, n ¼ 19) represent an attractive model for studying the mechanisms used by allopolyploids to ensure the diploid-like meiotic pairing pattern. In oilseed rape haploids, homeologous chromosome pairing at metaphase I was found to be genetically based and controlled by a major gene, PrBn, segregating in a background of polygenic variation. In this study, we have mapped PrBn within a 10-cM interval on the C genome linkage group DY15 and shown that PrBn displays incomplete penetrance or variable expressivity. We have identified three to six minor QTL/BTL that have slight additive effects on the amount of pairing at metaphase I but do not interact with PrBn. We have also detected a number of other loci that interact epistatically, notably with PrBn. Our results support the idea that, as in other polyploid species, metaphase I homeologous pairing in oilseed rape haploids is controlled by an integrated system of several genes, which function in a complex manner.

In allopolyploids, correct chromosome segregation requires suppression of non-homologous crossovers while levels of homologous crossovers are ensured. To date, no mechanism able to specifically inhibit non-homologous crossovers has been described in allopolyploids other than in bread wheat. Here, we show that reducing the number of functional copies of MSH4 , an essential gene for the main crossover pathway, prevents non-homologous crossovers in allotetraploid Brassica napus . We show that non-homologous crossovers originate almost exclusively from the MSH4 -dependent recombination pathway and that their numbers decrease when MSH4 returns to single copy in B. napus ; by contrast, homologous crossovers remain unaffected by MSH4 duplicate loss. We also demonstrate that MSH4 systematically returns to single copy following numerous independent polyploidy events, a pattern that is probably not by chance. These results suggest that stabilization of allopolyploid meiosis can be enhanced by loss of a key meiotic recombination gene.

As part of an ongoing research program dedicated to the understanding of proanthocyanidin (PA) accumulation in Brassica napus seed coat, transgenic rapeseed plants carrying a 2.3-kb fragment of the Arabidopsis thaliana BAN promoter (ProAtBAN) fused to the uidA reporter gene (GUS) were generated. Analysis of these plants revealed that ProAtBAN was activated in B. napus seed coat, following a spatio-temporal pattern that was very similar to the PA deposition profile in rapeseed and also to the one previously described in Arabidopsis. ProAtBAN activity occurred as soon as the early stages of embryogenesis and was restricted to the cells where PAs were shown to accumulate. Therefore, the Arabidopsis BAN promoter can be used to trigger gene expression in B. napus seed coat for both genetic engineering and functional validation of candidate genes. In addition, these data strongly suggest that the transcriptional regulatory network of the BAN gene is conserved between Arabidopsis and rapeseed. This is consistent with the fact that similarity searches of the public rapeseed sequence databases allowed recovering the rapeseed homologs for several BAN regulators, namely TT1, TT2, TT8, TT16 and TTG1, which have been previously described in Arabidopsis.