| 2. |
- Caldwell, Martyn M., et al.
(author)
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Terrestrial ecosystems, increased solar ultraviolet radiation and interactions with other climatic change factors
- 2003
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In: Photochemical and Photobiological Sciences. - : Springer Science and Business Media LLC. - 1474-9092 .- 1474-905X. ; 2:1, s. 29-38
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Research review (peer-reviewed)abstract
- Based on research to date, we can state some expectations about terrestrial ecosystem response as several elements of global climate change develop in coming decades. Higher plant species will vary considerably in their response to elevated UV-B radiation, but the most common general effects are reductions in height of plants, decreased shoot mass if ozone reduction is severe, increased quantities of some phenolics in plant tissues and, perhaps, reductions in foliage area. In some cases, the common growth responses may be lessened by increasing CO2 concentrations. However, changes in chemistry of plant tissues will generally not be reversed by elevated CO2. Among other things, changes in plant tissue chemistry induced by enhanced UV-B may reduce consumption of plant tissues by insects and other herbivores, although occasionally consumption may be increased. Pathogen attack on plants may be increased or decreased as a consequence of elevated UV-B, in combination with other climatic changes. This may be affected both by alterations in plant chemistry and direct damage to some pathogens. Water limitation may decrease the sensitivity of some agricultural plants to UV-B, but for vegetation in other habitats, this may not apply. With global warming, the repair of some types of UV damage may be improved, but several other interactions between warming and enhanced UV-B may occur. For example, even though warming may lead to fewer killing frosts, with enhanced UV-B and elevated CO2 levels, some plant species may have increased sensitivity to frost damage. Originally published by the United Nations Environment Programme (UNEP) in "Environmental Effects of Ozone Depletion and its Interactions with Climate Change: 2002 Assessment". See http://www.unep.org/ozone/Publications/index.asp and http://www.earthprint.com/show.htm
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| 3. |
- Kalbin, Georgi, et al.
(author)
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UV-B-induced DNA damage and expression of defence genes under UV-B stress : tissue-specific molecular marker analysis in leaves
- 2001
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In: Plant, Cell and Environment. - : Wiley. - 0140-7791 .- 1365-3040. ; 24:9, s. 983-990
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Journal article (peer-reviewed)abstract
- The aim of this study was to investigate the regulatory effect of ultraviolet-B (UV-B) radiation on a number of key stress response genes found in the epidermis and mesophyll of Pisum sativum L., Argenteum mutant. This mutant was chosen for the ease with which the entire epidermis can be removed from the mesophyll tissue. An additional goal was to explore the potential modifying effect of pre-acclimation of plants to UV-B radiation prior to exposure by UV-B during treatment. Results showed that mRNA accumulation was similar during acute short-term UV-B exposure for chalcone synthase (Chs) and short-chain alcohol dehydrogenase (SadA) in both epidermis and mesophyll. In contrast, the mRNA levels differed considerably between tissues for phenylalanine ammonia lyase, chalcone isomerase and lipid transfer protein. After 24 h incubation in visible light after cessation of UV-B exposure, the regulation of mRNA levels also differed between Chs and SadA, the former showing no expression in the epidermis and the latter none in the mesophyll. Acclimation to low UV-B levels before acute exposures resulted in delayed induction of Chs and SadA. Measurements of UV-B-induced cyclobutane pyrimidine dimers (CPDs) showed a greater formation in epidermis than in mesophyll. In addition, acclimation at low UV-B levels resulted in significantly higher basal levels of CPDs than in non-acclimated plants in both mesophyll and epidermis and also in increased damage in concomitant acute exposures. The lack of correlation between the number of CPDs and levels of transcripts for defence genes, indicates that DNA damage does not control transcription of these genes.
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