No abstract

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.

Pollen hydration on dry stigmas is strictly regulated by pollen–stigma interactions in the Brassicaceae. Although several related molecular events have been described, the molecular mechanism underlying pollen hydration remains elusive. Multiple B‐class pollen coat proteins (PCP‐Bs) are involved in pollen hydration. Here, by analyzing the interactions of two PCP‐Bs with three Arabidopsis thaliana stigmas strongly expressing S‐domain receptor kinase (SD‐RLK), we determined that SD‐RLK28 directly interacts with PCP‐Bβ. We investigated pollen hydration, pollen germination, pollen tube growth, and stigma receptivity in the sd‐rlk28 and pcp‐bβ mutants. PCP‐Bβ acts in the pollen to regulate pollen hydration on stigmas. Loss of SD‐RLK28 had no effect on pollen viability, and sd‐rlk28 plants had normal life cycles without obvious defects. However, pollen hydration on sd‐rlk28 stigmas was impaired and pollen tube growth in sd‐rlk28 pistils was delayed. The defect in pollen hydration on sd‐rlk28 stigmas was independent of changes in reactive oxygen species levels in stigmas. These results indicate that SD‐RLK28 functions in the stigma as a PCP‐Bβ receptor to positively regulate pollen hydration on dry stigmas.This article is protected by copyright. All rights reserved.