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AtROP1 negatively regulates potato resistance to Phytophthora infestans via NADPH oxidase-mediated accumulation of H(2)O(2)
BACKGROUND: Small GTPases are monomeric guanine nucleotide-binding proteins. In plants, ROPs regulate plant cell polarity, plant cell differentiation and development as well as biotic and abiotic stress signaling pathways. RESULTS: We report the subcellular localization of the AtRop1 protein at the...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4323192/ https://www.ncbi.nlm.nih.gov/pubmed/25547733 http://dx.doi.org/10.1186/s12870-014-0392-2 |
Sumario: | BACKGROUND: Small GTPases are monomeric guanine nucleotide-binding proteins. In plants, ROPs regulate plant cell polarity, plant cell differentiation and development as well as biotic and abiotic stress signaling pathways. RESULTS: We report the subcellular localization of the AtRop1 protein at the plasma membrane in tobacco epidermal cells using GFP fusions. Additionally, transient and stable expression of a dominant negative form (DN) of the Arabidopsis AtRop1 in potato led to H(2)O(2) accumulation associated with the reduced development of Phytophthora infestans Montagne de Bary and smaller lesions on infected potato leaves. The expression of the Strboh-D gene, a NADPH oxidase homologue in potato, was analyzed by RT-PCR. Expression of this gene was maintained in DN-AtRop1 transgenic plants after infection with P. infestans. In transgenic potato lines, the transcript levels of salicylic acid (SA) and jasmonic acid (JA) marker genes (Npr1 and Lox, respectively) were analyzed. The Lox gene was induced dramatically whereas expression of Npr1, a gene up-regulated by SA, decreased slightly in DN-AtRop1 transgenic plants after infection with P. infestans. CONCLUSIONS: In conclusion, our results indicate that DN-AtROP1 affects potato resistance to P. infestans. This is associated with increased NADPH oxidase-mediated H(2)O(2) production and JA signaling. |
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