Brassica napus (2n = 4x = 38, AACC) is an important allopolyploid crop derived from interspecific crosses between Brassica rapa (2n = 2x = 20, AA) and Brassica oleracea (2n = 2x = 18, CC). However, no truly wild B. napus populations are known; its origin and improvement processes remain unclear. Here, we resequence 588 B. napus accessions. We uncover that the A subgenome may evolve from the ancestor of European turnip and the C subgenome may evolve from the common ancestor of kohlrabi, cauliflower, broccoli, and Chinese kale. Additionally, winter oilseed may be the original form of B. napus. Subgenome-specific selection of defense-response genes has contributed to environmental adaptation after formation of the species, whereas asymmetrical subgenomic selection has led to ecotype change. By integrating genome-wide association studies, selection signals, and transcriptome analyses, we identify genes associated with improved stress tolerance, oil content, seed quality, and ecotype improvement. They are candidates for further functional characterization and genetic improvement of B. napus.
Stem rot caused by Sclerotinia sclerotiorum is one of the most devastating diseases of rapeseed (Brassica napus L.) which causes huge loss in rapeseed production. Genetic sources with high level of resistance has not been found in rapeseed. In this study, 68 accessions in six Brassica species, including 47 accessions of B. oleracea, were evaluated for leaf and stem resistance to S. sclerotiorum. Large variation of resistance was found in Brassica, with maximum differences of 5-and 57-folds in leaf and stem resistance respectively. B. oleracea, especially its wild types such as B. rupestris, B. incana, B. insularis, and B. villosa showed high level of resistance. Our data suggest that wild types of B. oleracea possess tremendous potential for improving S. sclerotiorum resistance of rapeseed.
The lack of resistant source has greatly restrained resistance breeding of rapeseed (Brassica napus, AACC) against Sclerotinia sclerotiorum which causes severe yield losses in rapeseed production all over the world. Recently, several wild Brassica oleracea accessions (CC) with high level of resistance have been identified (Mei et al. in Euphytica 177:393-400, 2011), bringing a new hope to improve Sclerotinia resistance of rapeseed. To map quantitative trait loci (QTL) for Sclerotinia resistance from wild B. oleracea, an F2 population consisting of 149 genotypes, with several clones of each genotypes, was developed from one F1 individual derived from the cross between a resistant accession of wild B. oleracea (B. incana) and a susceptible accession of cultivated B. oleracea var. alboglabra. The F2 population was evaluated for Sclerotinia reaction in 2009 and 2010 under controlled condition. Significant differences among genotypes and high heritability for leaf and stem reaction indicated that genetic components accounted for a large portion of the phenotypic variance. A total of 12 QTL for leaf resistance and six QTL for stem resistance were identified in 2 years, each explaining 2.2-28.4 % of the phenotypic variation. The combined effect of alleles from wild B. oleracea reduced the relative susceptibility by 22.5 % in leaves and 15 % in stems on average over 2 years. A 12.8-cM genetic region on chromosome C09 of B. oleracea consisting of two major QTL intervals for both leaf and stem resistance was assigned into a 2.7-Mb genomic region on chromosome A09 of B. rapa, harboring about 30 putative resistance-related genes. Significant negative corrections were found between flowering time and relative susceptibility of leaf and stem. The association of flowering time with Sclerotinia resistance is discussed.
Sclerotinia sclerotiorum is a devastating necrotrophic plant pathogen with a worldwide distribution. Cell wall-degrading enzymes and oxalic acid are important to the virulence of this pathogen. Here, we report a novel secretory protein, Ss-Rhs1, which is essential for the virulence of S. sclerotiorum. Ss-Rhs1 is believed to contain a typical signal peptide at the N-terminal and eight rearrangement hotspot (Rhs) repeats. Ss-Rhs1 exhibited a high level of expression at the initial stage of sclerotial development, as well as during the hyphal infection process. Targeted silencing of Ss-Rhs1 resulted in abnormal colony morphology and reduced virulence on host plants. Microscopic observations indicated that Ss-Rhs1-silenced strains exhibited reduced efficiency in compound appressoria formation.
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