135 resultados para Guilbert-Estevez
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Plant resistance to necrotrophic fungi is regulated by a complex set of signaling pathways that includes those mediated by the hormones salicylic acid (SA), ethylene (ET), jasmonic acid (JA), and abscisic acid (ABA). The role of ABA in plant resistance remains controversial, as positive and negative regulatory functions have been described depending on the plant-pathogen interaction analyzed. Here, we show that ABA signaling negatively regulates Arabidopsis (Arabidopsis thaliana) resistance to the necrotrophic fungus Plectosphaerella cucumerina. Arabidopsis plants impaired in ABA biosynthesis, such as the aba1-6 mutant, or in ABA signaling, like the quadruple pyr/pyl mutant (pyr1pyl1pyl2pyl4), were more resistant to P. cucumerina than wild-type plants. In contrast, the hab1-1abi1-2abi2-2 mutant impaired in three phosphatases that negatively regulate ABA signaling displayed an enhanced susceptibility phenotype to this fungus. Comparative transcriptomic analyses of aba1-6 and wild-type plants revealed that the ABA pathway negatively regulates defense genes, many of which are controlled by the SA, JA, or ET pathway. In line with these data, we found that aba1-6 resistance to P. cucumerina was partially compromised when the SA, JA, or ET pathway was disrupted in this mutant. Additionally, in the aba1-6 plants, some genes encoding cell wall-related proteins were misregulated. Fourier transform infrared spectroscopy and biochemical analyses of cell walls from aba1-6 and wild-type plants revealed significant differences in their Fourier transform infrared spectratypes and uronic acid and cellulose contents. All these data suggest that ABA signaling has a complex function in Arabidopsis basal resistance, negatively regulating SA/JA/ET-mediated resistance to necrotrophic fungi.
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Sign.: []4, A-D4, E1
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Acknowledgements Gokul Gopalan (a Senior Global Medical Director [Respiratory], at Teva Pharmaceuticals, Frazer, PA, US, at the time of this study), assisted with study design. Funding Funds to acquire the dataset from the Pharmo Institute for Drug Outcomes Research (Utrecht, the Netherlands) were provided by RiRL. The study received institutional support from Teva Pharmaceuticals Europe B.V. Gokul Gopalan, a Senior Global Medical Director (Respiratory), at Teva Pharmaceuticals, Frazer, PA, US, at the time of this study, assisted with study design, but neither Teva Pharmaceuticals Europe B.V. nor Teva Pharmaceuticals, Frazer, PA, US, contributed, either in part or in whole, to the collection, analysis, or interpretation of study data, manuscript writing, or the decision to submit the manuscript for publication. Erratum The original version of this article unfortunately contained errors that have since been corrected. The word “pharmo” has been fully capitalised to “PHARMO” throughout the article. The reference to Table 2 in the first and second sentence under the Outcomes heading has been replaced with Fig. 3. Under the Abbreviations heading ‘extrafine-particle’ was repeated, this has been corrected to ‘EF-HFA-BDP [Qvar®]: extrafine-particle hydrofluoroalkane beclomethasone dipropionate’. The competing interests of Nicolas Roche and Theresa Guibert have been amended. Academic affiliations for Dirkje S. Postma (2), Richard J. Martin (3), Ron M.C. Herrings (4), Jetty Overbeek (4), and Nicolas Roche (7) have been corrected. Figure 3 in the online and pdf version did not match, this been amended
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Contiene : Tom. 3.
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French and English words.
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