The depletion of stratospheric ozone by chlorofluorocarbons has increased the UV-B fluence rates over the Earth during the past 2 decades, and it is feared that the increased UV-B radiation might affect plant production. High UV-B irradiance can cause various forms of damage in any organism. In plants, UV light damages DNA and photosynthetic machinery and generates reactive oxygen species that damage macromolecules. However, low UV-B fluence rates can stimulate the transduction of signals that regulate the plant”Ēs protective response. Some of these UV-B responses are activated not by DNA damage, but specifically by radiation in the UV-B range (280-320 nm), and regulate the expression a wide range of genes. Therefore, it is important that we understand how signal transduction leads to the regulation of expression of genes that mediate protection against UV-B light. We tried to isolate rice genes that cause hypersensitivity to low UV-B irradiation by looking for the inhibition of hypocotyl elongation by UV-B doses below the level that triggers damage responses in plants (1).
T2 rice FOX Arabidopsis seedlings were grown for 24 h in the dark, irradiated with UV-B light (FL-20 SE) at 3 W/m2 for 5 min through a plastic plate as UV-C filter, and then returned to the dark. This treatment was repeated after 24 h. We measured the hypocotyl elongation 24 h later and selected seedlings with shorter hypocotyls than Col. as candidate hypersensitive mutants. We checked that 1 h of UV-A irradiation after each UV-B pulse did not affect the hypocotyl length of wild-type plants. This UV-A treatment was included to activate the photolyases that repair DNA damage. Although we isolated many candidate hypersensitive mutants, some showed short hypocotyls not due to UV response.
1. Suesslin C, Frohnmeyer H. An Arabidopsis mutant defective in UV-B light-mediated responses. Plant Journal 33, 591-601 (2003).