QTL mapping and transcriptome analysis identify novel QTLs and candidate genes in Brassica villosa for quantitative resistance against Sclerotinia sclerotiorum

KEY MESSAGE: Novel QTLs and candidate genes for Sclerotinia-resistance were identified in B. villosa , a wild Brassica species, which represents a new genetic source for improving oilseed rape resistance to SSR. ABSTRACT: Sclerotinia stem rot (SSR), caused by Sclerotinia sclerotiorum, is one of the most destructive diseases in oilseed rape growing regions. To date, there is no effective genetic resistance against S. sclerotiorum in the B. napus germplasm and knowledge of the molecular plant–fungal interaction is also limited. To identify new resistance resources, we screened a set of wild Brassica species and identified B. villosa (BRA1896) with a high level of Sclerotinia-resistance. Two segregating F(2) populations for Sclerotinia-resistance, generated by interspecific crosses between the resistant B. villosa (BRA1896) and the wild susceptible B. oleracea (BRA1909) were assessed for Sclerotinia-resistance. Genetic mapping using a 15-k Illumina Infinium SNP-array resulted in a high-density genetic map containing 1,118 SNP markers and spanning a total genetic length of 792.2 cM. QTL analysis revealed seven QTLs explaining 3.8% to 16.5% of phenotypic variance. Intriguingly, RNAseq-based transcriptome analysis identified genes and pathways specific to B. villosa, of which a cluster of five genes encoding putative receptor-like kinases (RLKs) and two pathogenesis-related (PR) proteins are co-localized within a QTL on chromosome C07. Furthermore, transcriptomic analysis revealed enhanced ethylene (ET)-activated signaling in the resistant B. villosa, which is associated with a stronger plant immune response, depressed cell death, and enhanced phytoalexin biosynthesis compared to the susceptible B. oleracea. Our data demonstrates that B. villosa represents a novel and unique genetic source for improving oilseed rape resistance against SSR. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00122-023-04335-9.