Authors: Michael Pröbsting, Dirk Schenke, Roxana Hossain, Claudia Häder, Tim Thurau, Lisa Wighardt, Andrea Schuster, Zheng Zhou, Wanzhi Ye, Steffen Rietz, Gunhild Leckband, Daguang Cai
Published: 2020-05-02
DOI: 10.1111/pbi.13394
Source: Full article
SummaryBrassica napusis highly susceptible towardsVerticillium longisporum(Vl43) with no effective genetic resistance. It is believed that the fungus reprogrammes plant physiological processes by up‐regulation of so‐called susceptibility factors to establish a compatible interaction. By transcriptome analysis, we identified genes, which were activated/up‐regulated in rapeseed afterVl43infection. To test whether one of these genes is functionally involved in the infection process and loss of function would lead to decreased susceptibility, we firstly challenged KO lines of corresponding Arabidopsis orthologs withVl43and compared them with wild‐type plants. Here, we report that the KO ofAtCRT1aresults in drastically reduced susceptibility of plants toVl43. To provecrt1amutation also decreases susceptibility inB. napus, we identified 10 mutations in a TILLING population. Three T3 mutants displayed increased resistance as compared to the wild type. To validate the results, we generated CRISPR/Cas‐inducedBnCRT1amutants, challenged T2 plants withVl43and observed an overall reduced susceptibility in 3 out of 4 independent lines. Genotyping by allele‐specific sequencing suggests a major effect of mutations in theCRT1aA‐genome copy, while the C‐genome copy appears to have no significant impact on plant susceptibility when challenged withVl43. As revealed by transcript analysis, the loss of function ofCRT1aresults in activation of the ethylene signalling pathway, which may contribute to reduced susceptibility. Furthermore, this study demonstrates a novel strategy with great potential to improve plant disease resistance.