Cell death regulation but not abscisic acid signaling is required for enhanced immunity to Botrytis in Arabidopsis cuticle-permeable mutants
© The Author(s) 2019. Published by Oxford University Press on behalf of the Society for Experimental Biology.
| Publié dans: | Journal of experimental botany. - 1985. - 70(2019), 20 vom: 24. Okt., Seite 5971-5984 |
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| Auteur principal: | |
| Autres auteurs: | , , , , , , |
| Format: | Article en ligne |
| Langue: | English |
| Publié: |
2019
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| Accès à la collection: | Journal of experimental botany |
| Sujets: | Journal Article Research Support, Non-U.S. Gov't Botrytis cinerea BOS1 ERA1 RNA sequencing cell death cuticle permeable farnesyl transferase immunity plus... |
| Résumé: | © The Author(s) 2019. Published by Oxford University Press on behalf of the Society for Experimental Biology. Prevailing evidence indicates that abscisic acid (ABA) negatively influences immunity to the fungal pathogen Botrytis cinerea in most but not all cases. ABA is required for cuticle biosynthesis, and cuticle permeability enhances immunity to Botrytis via unknown mechanisms. This complex web of responses obscures the role of ABA in Botrytis immunity. Here, we addressed the relationships between ABA sensitivity, cuticle permeability, and Botrytis immunity in the Arabidopsis thaliana ABA-hypersensitive mutants protein phosphatase2c quadruple mutant (pp2c-q) and enhanced response to aba1 (era1-2). Neither pp2c-q nor era1-2 exhibited phenotypes predicted by the known roles of ABA; conversely, era1-2 had a permeable cuticle and was Botrytis resistant. We employed RNA-seq analysis in cuticle-permeable mutants of differing ABA sensitivities and identified a core set of constitutively activated genes involved in Botrytis immunity and susceptibility to biotrophs, independent of ABA signaling. Furthermore, botrytis susceptible1 (bos1), a mutant with deregulated cell death and enhanced ABA sensitivity, suppressed the Botrytis immunity of cuticle permeable mutants, and this effect was linearly correlated with the extent of spread of wound-induced cell death in bos1. Overall, our data demonstrate that Botrytis immunity conferred by cuticle permeability can be genetically uncoupled from PP2C-regulated ABA sensitivity, but requires negative regulation of a parallel ABA-dependent cell-death pathway |
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| Description: | Date Completed 17.08.2020 Date Revised 17.08.2020 published: Print Citation Status MEDLINE |
| ISSN: | 1460-2431 |
| DOI: | 10.1093/jxb/erz345 |