Host alternative NADH:ubiquinone oxidoreductase serves as susceptibility factor to promote pathogenesis of Rhizoctonia solani in plants
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Title |
Host alternative NADH:ubiquinone oxidoreductase serves as susceptibility factor to promote pathogenesis of Rhizoctonia solani in plants
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Creator |
Kant, Ravi
Tyagi, Kriti Ghosh, Srayan Jha, Gopaljee |
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Subject |
Rhizoctonia solani
ubiquinone oxidoreductase NADH pathogenesis susceptibility factor |
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Description |
Accepted date: 6 June 2019
Phytopathogens have evolved mechanisms to utilize host genes (commonly known as susceptibility factors) to promote its pathogenesis. Rhizoctonia solani is one of the highly destructive fungal pathogens of various plants, including rice. Previously we had reported differentially regulated rice genes during pathogenesis of R. solani. In this study, we analyzed the role of tomato homologs of two of the rice genes i.e Isoflavone reductase (IFR) and alternative NADH:ubiquinone oxidoreductase (NUOR) as potential susceptibility factors for R. solani. Virus induced gene silencing (VIGS) of NUOR gene in tomato resulted in compromised susceptibility against R. solani, while IFR-silenced plants demonstrated susceptibility similar to that of control plants. NUOR silencing in tomato led to homogenous accumulation of reactive oxygen species (ROS) (optimum range) upon R. solani infection. In addition, expression and enzyme activities of some of the host defense and anti-oxidant genes were enhanced, while H2O2 content, lipid peroxidation and electrolyte leakage were reduced in NUOR-silenced plants. Similarly, transient silencing of OsNUOR gene provided tolerance against R. solani infection in rice. Overall, the data presented in this study suggests that NUOR serves as a host susceptibility factor to promote pathogenesis of R. solani. RK is supported by N-PDF fellowship from SERB, (DST, Govt. of India), KT is supported by senior research fellowship from Department of Biotechnology (Govt. of India) and SG is supported by SPM fellowship from Council of Scientific and Industrial Research (Govt. of India). We would thank Dr. Senthil-Kumar Muthappa from NIPGR, New Delhi for providing us the pTRV (pTRV1+pTRV2) plasmids. We acknowledge the assistance of central instrumentation facilities, NIPGR, New Delhi. This work was supported by core research grant from the National Institute of Plant Genome Research, India and research funding from DBT, Government of India. |
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Date |
2019-07-22T11:13:55Z
2019-07-22T11:13:55Z 2019 |
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Type |
Article
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Identifier |
Phytopathology, 109(10): 1741-1750
1943-7684 http://223.31.159.10:8080/jspui/handle/123456789/962 https://apsjournals.apsnet.org/doi/10.1094/PHYTO-02-19-0055-R https://doi.org/10.1094/PHYTO-02-19-0055-R |
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Language |
en_US
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Format |
application/pdf
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Publisher |
American Phytopathological Society
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