Plants respond to both abiotic and biotic stresses with alterations in the expression of genes required to produce protective metabolites. Sometimes plants can be challenged with different stresses simultaneously and as they cannot evade from this situation, priorities have to be set to deal with the most urgent threat. The abiotic stress ultraviolet‐B (UV‐B) light induces the production of UV‐protective flavonols in Arabidopsis Col‐0 cell suspension cultures and this accumulation is attenuated by concurrent application of the bacterial elicitor flg22 (simulating biotic stress). This inhibition correlates with strong suppression of the flavonol biosynthesis genes. In parallel, flg22 induces the production of defence‐related compounds, such as the phytoalexins, camalexin and scopoletin, as well as lignin, a structural barrier thought to restrict pathogen spread. This correlated positively with flg22‐mediated expression of enzymes for lignin, scopoletin and camalexin production. As flavonols, lignin and scopoletin are all derived from phenylalanine, it appears that the plant focuses the metabolism on production of scopoletin and lignin at the expense of flavonol production. Furthermore, it appears that this crosstalk involves antagonistic regulation of two opposing MYB transcription factors, the positive regulator of the flavonol pathway MYB12 (UV‐B‐induced and flg22‐suppressed) and the negative regulator MYB4 (UV‐B‐ and flg22‐induced).

Current crop production systems are prone to increasing pathogen pressure. Fundamental understanding of molecular plant-pathogen interactions, the availability of crop and pathogen genomic information, as well as emerging genome editing permits a novel approach for breeding of crop disease resistance. We describe here strategies to identify new targets for resistance breeding with focus on interruption of the compatible plant-pathogen interaction by CRISPR/Cas-mediated genome editing. Basically, crop genome editing can be applied in several ways to achieve this goal. The most common approach focuses on the “simple” knockout by non-homologous end joining repair of plant susceptibility factors required for efficient host colonization. However, genome re-writing via homology-directed repair or base editing can also prevent host manipulation by changing the targets of pathogen-derived effectors or molecules beyond recognition, which also decreases plant susceptibility. We conclude that genome editing by CRISPR/Cas will become increasingly indispensable to generate in relatively short time beneficial resistance traits in crops to meet upcoming challenges.

Summary: Brassica 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.

Arabidopsis nuclear- and chloroplast-localized WHIRLY1 adjusts SA content in cells via ICS1, PAL1, and BSMT1 to regulate plant senescence in a developmental-dep