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The study of plant-virus interactions requires a method which enables not only the detection of virus presence, but also its distribution in the infected plant tissue. We adopted a tissue print immunoblot technique for localization of potato virus Y (PVY) coat protein (CP) in infected potato and tobacco tissue. In potato stem cross-sections PVY CP was detected on the whole surface of the prints, however significantly higher concentration was observed in epidermis and phloem tissue. In the petiole of infected tobacco leaves the presence of viral protein was confined mainly to peripheral layers of parenchyma and epidermis. In phloem tissue the signal was also visible but it was significantly weaker. In our hands this approach is highly specific and gives resolution on the level of individual cells, thus it can be applied in several fields. As potyviral capsid proteins are involved in several events of pathogenesis the technique for immunolocalization of PVY CP could provide information which will shed new light on the virology of PVY.
Previous studies argue that salicylic acid (SA) plays an important role in the plant signal transduction pathway(s) leading to disease resistance. It has been proposed that one of its modes of action is inhibition of catalase and elevation of H₂O₂ level in the tissue. To verify the role of SA and H₂O₂ during pathogenesis, transgenic tobacco plants expressing Saccharomyces cerevisiae CTA1 gene coding for peroxisomal catalase were constructed. These plants possess 2-4-fold higher total catalase activity under normal growth conditions. No symptoms of chlorosis and/or necrosis were observed. Levels of pathogenesis-related proteins (PR) and their respective mRNAs were significantly reduced in the infected leaves of the transgenic plants. No change in PR expression was detected in uninfected leaves of both CTA1 and control plants challenged with TMV. These results suggest that elevation in catalase activity and resulting reduction of H₂O₂ level results in more severe local disease symptoms, apparently due to alteration of the hypersensitive response mechanism and does not influence systemic acquired resistance after viral infection.
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