ArticleMolecular plant pathology2022
The exodomain of the impaired oomycete susceptibility 1 receptor mediates both endoplasmic reticulum stress responses and abscisic acid signalling during downy mildew infection of Arabidopsis.
Article in Molecular plant pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 4 citations in OpenAlex.
- Multiomics analyses of mutants for Marchantia polymorpha FERONIA and MARIS reveal a link between cell wall integrity and abscisic acid responses.Plant & cell physiology · 2026Article
- Multi-model GWAS reveals key loci for leaf angle in maize inbred lines from southeast China.BMC plant biology · 2026Article
- Role of PMR4 and PDLP1 in priming of early acting penetration defense by resistance-inducing β-amino acids.iScience · 2024Article
- The exodomain of the impaired oomycete susceptibility 1 receptor mediates both endoplasmic reticulum stress responses and abscisic acid signalling during downy mildew infection of Arabidopsis.Molecular plant pathology · 2022Article
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5 authors at 1 institution in 1 country.
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Abstract
The phytohormone abscisic acid (ABA) regulates cell growth and plant development, and contributes to defence responses to pathogens. We previously showed that the Arabidopsis malectin-like domain leucine-rich repeat receptor-like kinase (MLD-LRR-RLK) impaired oomycete susceptibility 1 (IOS1) attenuates ABA signalling during infection with the oomycete downy mildew pathogen Hyaloperonospora arabidopsidis. The exodomain of IOS1 with its MLD retains the receptor in the endoplasmic reticulum (ER), where it interacts with the ribophorin HAP6 to dampen a pathogen-induced ER stress response called the unfolded protein response (UPR). The down-regulation of both ABA and UPR signalling probably provides the pathogen with an advantage for infection. Here, we show that ABA-related phenotypes of the ios1-1 mutant, such as up-regulated expression of ABA-responsive genes and hypersensitivity to exogenous ABA application, were reverted by expression of the IOS1 exodomain in the mutant background. Furthermore, knockdown mutants for ER-resident HAP6 showed similarly reduced UPR and ABA signalling, indicating that HAP6 positively regulates both pathways. Our data suggest that the IOS1 exodomain and HAP6 contribute in the ER to the IOS1-mediated interference with ABA and UPR signalling.
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