LESION MIMIC MUTANT 1 confers basal resistance to Sclerotinia sclerotiorum in rapeseed via a salicylic acid-dependent pathway.

Rapeseed (Brassica napus) is a major edible oilseed crop consumed worldwide. However, its yield is seriously affected by infection from the broad-spectrum non-obligate pathogen Sclerotinia sclerotiorum due to a lack of highly resistant germplasm. Here, we identified a Sclerotinia-resistant and light-dependent lesion mimic mutant from an EMS-mutagenized population of the rapeseed inbred Zhongshuang 11 (ZS11) named lesion mimic mutant 1 (lmm1). The phenotype of lmm1 is controlled by a single recessive gene, which mapped onto chromosome C04 by bulked segregant analysis (BSA) within a 2.71-Mb interval. Histochemical analysis indicated that H2O2 strongly accumulated and cell death occurred around the lesion mimic spots. Among 877 differentially expressed genes (DEGs) between ZS11 and lmm1 leaves, 188 DEGs were enriched in the defense response, including 95 DEGs involved in systemic acquired resistance (SAR), which is consistent with the higher salicylic acid levels in lmm1. Combining of BSA and transcriptome, we identified a significantly up-regulated gene BnaC4.PR2, which encodes β-1,3-glucanase, as the candidate gene. Overexpression of BnaC4.PR2 may induce reactive oxygen species burst to trigger partial cell death and SAR. Our study provides a new genetic resource for S. sclerotiorum resistance as well as fresh insights into disease resistance breeding in B. napus.