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      Alterations in rice chloroplast integrity, photosynthesis and metabolome associated with pathogenesis of Rhizoctonia solani

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      Scientific Reports
      Nature Publishing Group

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          Abstract

          Sheath blight disease is caused by a necrotrophic fungal pathogen Rhizoctonia solani and it continues to be a challenge for sustainable rice cultivation. In this study, we adopted a multi-pronged approach to understand the intricacies of rice undergoing susceptible interactions with R. solani. Extensive anatomical alteration, chloroplast localized ROS, deformed chloroplast ultrastructure along with decreased photosynthetic efficiency were observed in infected tissue. GC-MS based metabolite profiling revealed accumulation of glycolysis and TCA cycle intermediates, suggesting enhanced respiration. Several aromatic and aliphatic amino acids along with phenylpropanoid intermediates were also accumulated, suggesting induction of secondary metabolism during pathogenesis. Furthermore, alterations in carbon metabolism along with perturbation of hormonal signalling were highlighted in this study. The gene expression analysis including RNAseq profiling reinforced observed metabolic alterations in the infected tissues. In conclusion, the present study unravels key events associated during susceptible rice- R. solani interactions and identifies metabolites and transcripts that are accumulated in infected tissues.

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          MS-DIAL: Data Independent MS/MS Deconvolution for Comprehensive Metabolome Analysis

          Data-independent acquisition (DIA) in liquid chromatography tandem mass spectrometry (LC-MS/MS) provides more comprehensive untargeted acquisition of molecular data. Here we provide an open-source software pipeline, MS-DIAL, to demonstrate how DIA improves simultaneous identification and quantification of small molecules by mass spectral deconvolution. For reversed phase LC-MS/MS, our program with an enriched LipidBlast library identified total 1,023 lipid compounds from nine algal strains to highlight their chemotaxonomic relationships.
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            Reprogramming a maize plant: transcriptional and metabolic changes induced by the fungal biotroph Ustilago maydis.

            The fungal pathogen Ustilago maydis establishes a biotrophic relationship with its host plant maize (Zea mays). Hallmarks of the disease are large plant tumours in which fungal proliferation occurs. Previous studies suggested that classical defence pathways are not activated. Confocal microscopy, global expression profiling and metabolic profiling now shows that U. maydis is recognized early and triggers defence responses. Many of these early response genes are downregulated at later time points, whereas several genes associated with suppression of cell death are induced. The interplay between fungus and host involves changes in hormone signalling, induction of antioxidant and secondary metabolism, as well as the prevention of source leaf establishment. Our data provide novel insights into the complexity of a biotrophic interaction.
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              Oxidative stress increased respiration and generation of reactive oxygen species, resulting in ATP depletion, opening of mitochondrial permeability transition, and programmed cell death.

              Mitochondria constitute a major source of reactive oxygen species and have been proposed to integrate the cellular responses to stress. In animals, it was shown that mitochondria can trigger apoptosis from diverse stimuli through the opening of MTP, which allows the release of the apoptosis-inducing factor and translocation of cytochrome c into the cytosol. Here, we analyzed the role of the mitochondria in the generation of oxidative burst and induction of programmed cell death in response to brief or continuous oxidative stress in Arabidopsis cells. Oxidative stress increased mitochondrial electron transport, resulting in amplification of H(2)O(2) production, depletion of ATP, and cell death. The increased generation of H(2)O(2) also caused the opening of the MTP and the release of cytochrome c from mitochondria. The release of cytochrome c and cell death were prevented by a serine/cysteine protease inhibitor, Pefablock. However, addition of inhibitor only partially inhibited the H(2)O(2) amplification and the MTP opening, suggesting that protease activation is a necessary step in the cell death pathway after mitochondrial damage.
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                Author and article information

                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group
                2045-2322
                06 February 2017
                2017
                : 7
                : 41610
                Affiliations
                [1 ]Plant microbe interactions laboratory, National Institute of Plant Genome Research, Aruna Asaf Ali Marg , New Delhi-110067, India
                Author notes
                [*]

                These authors contributed equally to this work.

                Article
                srep41610
                10.1038/srep41610
                5292701
                28165003
                9fab6dc8-fe93-4c15-ad55-d0dd47763106
                Copyright © 2017, The Author(s)

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                : 06 July 2016
                : 21 December 2016
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