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Tobacco susceptibility to Potato virus Y-NTN infection is affected by grafting and endogenous cytokinin content

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    0446882 - ÚEB 2016 RIV IE eng J - Journal Article
    Spoustová, Petra - Hýsková, V. - Müller, Karel - Schnablová, Renáta - Ryšlavá, H. - Čeřovská, Noemi - Malbeck, Jiří - Cvikrová, Milena - Synková, Helena
    Tobacco susceptibility to Potato virus Y-NTN infection is affected by grafting and endogenous cytokinin content.
    Plant Science. Roč. 235, JUN 2015 (2015), s. 25-36. ISSN 0168-9452. E-ISSN 1873-2259
    Institutional support: RVO:61389030
    Keywords : Cytokinin * ipt gene * Antioxidant system
    Subject RIV: EF - Botanics
    Impact factor: 3.362, year: 2015

    Faster or stronger response to pathogen occurs if plants undergo prior priming. Cytokinins seem to be also involved in plant priming and in response to pathogens. Susceptibility to Potato virus Y-NTN RVYNTN was studied in transgenic cytokinin overproducing (Pssu-ipt) tobacco and compared with nontransgenic plants. Since cytokinin overproduction inhibits development of plant roots and grafting overcomes this limitation, both types were grown as rooted and/or grafted plants to check also the effect of grafting. Control rooted tobacco (C), the most susceptible to PVYNTN, showed always symptoms during the infection together with the rising virus content and a systemic response, such as accumulation of H2O2, salicylic acid (SA) and other phenolic acids, and stress-induced enzyme activities. In transgenic and grafted plants, the response to PVYNTN was dependent on protective mechanisms activated prior to the inoculation. In Pssu-ipt tobacco, cytokinin active forms and SA contents exceeded manifold their content in C. Grafting promoted the accumulation of phenolics, but SA, and stimulated peroxidase activities. Thus, the pre-infection barrier established in both transgenic and grafted plants helped to suppress partly the virus multiplication and resulted in milder symptom development. However, only the synergic effect of both grafting and the high cytokinins led to PVYNTN tolerance in transgenic grafts. Possible mechanisms were discussed.
    Permanent Link: http://hdl.handle.net/11104/0248843

     
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