New papers from Hückelhoven, Mayer and Vlot Labs.
Bacteria-triggered systemic immunity in barley is not a canonical systemic acquired resistance but is associated with WRKY and ETHYLENE RESPONSIVE FACTORs.
Sanjukta Dey , Marion Wenig, Gregor Langen, Sapna Sharma, Karl Kugler, Claudia Knappe, Bettina Hause, Marlies Bichlmeier, Valiollah Babaeizad, Jafargholi Imani, Ingar Janzik, Thomas Stempfl, Ralph Hückelhoven, Karl-Heinz Kogel, Klaus FX Mayer, Corina Vlot (2014)
Leaf-to-leaf, systemic immune signaling known as systemic acquired resistance (SAR) is poorly understood in monocotyledonous plants. Here, we characterize systemic immunity in barley (Hordeum vulgare) triggered after primary leaf infection with either Pseudomonas syringae pathovar japonica (Psj) or Xanthomonas translucens pathovar cerealis (Xtc). Both pathogens induced resistance in systemic, uninfected leaves against a subsequent challenge infection with Xtc. In contrast to SAR in Arabidopsis thaliana, systemic immunity in barley was not associated with NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 or the local or systemic accumulation of salicylic acid (SA). Instead, we documented a moderate local but not systemic induction of abscisic acid (ABA) after infection of leaves with Psj. In contrast to SA or its functional analog benzothiadiazole, local applications of the jasmonic acid methyl ester or ABA triggered systemic immunity to Xtc. RNA-seq analysis of local and systemic transcript accumulation revealed unique gene expression changes in response to both Psj and Xtc and a clear separation of local from systemic responses. The systemic response appeared relatively modest and quantitative RT-PCR associated systemic immunity with the local and systemic induction of two WRKY and two ETHYLENE RESPONSIVE FACTOR-like transcription factors. Systemic immunity against Xtc was further associated with transcriptional changes after a secondary/systemic Xtc challenge infection; these changes were dependent on the primary treatment. Taken together, bacteria-induced systemic immunity in barley may be mediated in part by WRKY and ERF-like transcription factors possibly facilitating transcriptional reprogramming to potentiate immunity.
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The receptor kinase IMPAIRED OOMYCETE SUSCEPTIBILITY 1 attenuates abscisic acid responses in Arabidopsis thaliana.
Plant Physiol. 166: 1506-1518.
Sophie Hok, Valérie Allasia, Emilie Andrio, Elodie Naessens, Elsa Ribes, Franck Panabières, Agnès Attard, Nicolas Ris, Mathilde Clément, Xavier Barlet, Yves Marco, Erwin Grill, Ruth Eichmann, Corina Weis, Ralph Hückelhoven, Alexandra Ammon, Jutta Ludwig-Müller, Lars M. Voll, Harald Keller (2014)
In plants, membrane-bound receptor kinases are essential for developmental processes, immune responses to pathogens and the establishment of symbiosis. We previously identified the Arabidopsis (Arabidopsis thaliana) receptor kinase IMPAIRED OOMYCETE SUSCEPTIBILITY 1 (IOS1) as required for successful infection with the downy mildew pathogen, Hyaloperonospora arabidopsidis. We report here that IOS1 is also required for full susceptibility of Arabidopsis to unrelated (hemi-)biotrophic filamentous oomycete and fungal pathogens. Impaired susceptibility in the absence of IOS1 appeared to be independent of plant defense mechanism. Instead, we found that ios1-1 plants were hypersensitive to the plant hormone abscisic acid (ABA), displaying enhanced ABA-mediated inhibition of seed germination, root elongation, and stomatal opening. These findings suggest that IOS1 negatively regulates ABA signaling in Arabidopsis. The expression of ABA-sensitive COR and RD genes was diminished in Arabidopsis during infection. This effect on ABA signaling was alleviated in the ios1-1 mutant background. Accordingly, ABA-insensitive and ABA-hypersensitive mutants were more susceptible and resistant to oomycete infection, respectively, showing that the intensity of ABA signaling affects the outcome of downy mildew disease. Taken together, our findings suggest that filamentous (hemi-)biotrophs attenuate ABA signaling in Arabidopsis during the infection process, and that IOS1 participates in this pathogen-mediated reprogramming of the host.
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The effective papilla hypothesis.
Ralph Hückelhoven (2014)
No abstract is available for this article.
