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Ozone-Response Mechanisms in Tobacco: Implications of Polyamine Metabolism

• Polyamines have been suggested to counteract oxidative damage in plants. Here, we present a detailed analysis of polyamine accumulation and its relationship to photosynthetic parameters in two tobacco (Nicotiana tabacum) cultivars (ozone-sensitive Bel W3 and ozone-tolerant Bel B) after a single oz...

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Bibliographic Details
Published in:The New phytologist 2002-12, Vol.156 (3), p.389-398
Main Authors: van Buuren, Marianne Louise, Guidi, Lucia, Fornalè, Silvia, Ghetti, Francesca, Franceschetti, Marina, Soldatini, Gian Franco, Bagni, Nello
Format: Article
Language:English
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Summary:• Polyamines have been suggested to counteract oxidative damage in plants. Here, we present a detailed analysis of polyamine accumulation and its relationship to photosynthetic parameters in two tobacco (Nicotiana tabacum) cultivars (ozone-sensitive Bel W3 and ozone-tolerant Bel B) after a single ozone pulse and after a 1-month exposure in the open air. • Free putrescine accumulated in undamaged tissue of both cultivars, whereas putrescine conjugated to soluble and cell-wall bound components accumulated predominantly in tissue undergoing cell death in Bel W3 plants. Accumulation was caused by a redirection of the conjugation pathway, as well as by a transient increase in arginine decarboxylase and ornithine decarboxylase specific activity. This increase seemed to be regulated at post-transcriptional level. • Measurements of chlorophyll content and fluorescence showed that, in addition to visible necrotic lesions, Bel W3 plants suffered considerable photosynthetic damage in other parts of the leaf. • Accumulation of conjugated putrescine is part of the ozone-induced programmed cell death response in Bel W3 plants. Ozone-induced synthesis of free putrescine is not correlated with ozone-resistance in Bel B plants, which are apparently impaired in signal transduction pathways that are necessary to control the cellular redox state. However, Bel B plants are able to perceive ozone stress and to induce a series of defense mechanisms without activating hypersensitive cell death.
ISSN:0028-646X
1469-8137
DOI:10.1046/j.1469-8137.2002.00539.x