UV-B-induced DNA damage and expression of defence genes under UV-B stress:tissue-specific molecular marker analysis in leaves

Citation
G. Kalbin et al., UV-B-induced DNA damage and expression of defence genes under UV-B stress:tissue-specific molecular marker analysis in leaves, PL CELL ENV, 24(9), 2001, pp. 983-990
Citations number
43
Categorie Soggetti
Plant Sciences","Animal & Plant Sciences
Journal title
PLANT CELL AND ENVIRONMENT
ISSN journal
01407791 → ACNP
Volume
24
Issue
9
Year of publication
2001
Pages
983 - 990
Database
ISI
SICI code
0140-7791(200109)24:9<983:UDDAEO>2.0.ZU;2-D
Abstract
The aim of this study was to investigate the regulatory effect of ultraviol et-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 fro m the mesophyll tissue. An additional goal was to explore the potential mod ifying effect of pre-acclimation of plants to UV-B radiation prior to expos ure by UV-B during treatment. Results showed that mRNA accumulation was sim ilar during acute short-term UV-B exposure for chalcone synthase (Chs) and short-chain alcohol dehydrogenase (SadA) in both epidermis and mesophyll. I n contrast, the mRNA levels differed considerably between tissues for pheny lalanine ammonia lyase, chalcone isomerase and lipid transfer protein. Afte r 24 h incubation in visible light after cessation of UV-B exposure, the re gulation of mRNA levels also differed between Chs and SadA, the former show ing no expression in the epidermis and the latter none in the mesophyll. Ac climation to low UV-B levels before acute exposures resulted in delayed ind uction of Chs and SadA. Measurements of UV-B-induced cyclobutane pyrimidine dimers (CPDs) showed a greater formation in epidermis than in mesophyll. I n addition, acclimation at low UV-B levels resulted in significantly higher basal levels of CPDs than in non-acclimated plants in both mesophyll and e pidermis and also in increased damage in concomitant acute exposures. The l ack 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.