Involvement and Non-Involvement of Pyrimidine Dimer Formation in UV-B Effects on Sorghum bicolor Moench Seedlings

Abstract

In plants ultraviolet B (UV-B) radiation causes not only DNA lesion and other deleterious effects, but also assumingly contributes to normal photomorphogenesis mediated by a putative UV-B photoreceptor(s). In order to examine which UV-B effects do or do not involve DNA lesion, cyclobutane pyrimidine dimers (CPDs), thymine dimer (CTD), and pyrimidine (6-4) pyrimidinone photoproducts (6-4PP) were determined by enzyme-linked immunosorbent assay or radioimmunoassay with regard to UV-B-induced anthocyanin synthesis and inhibition as well as coil formation (abnormal growth) of the first internode of Sorghum bicolor Moench. For anthocyanin, dark-grown 3-day-old seedlings were irradiated at various fluences with each of the three UV radiations having bands of (A) 295-345, (B) 300-350, and (C) 325-385 nm at 1/4 peak height, followed by far-red light (FR) to exclude phytochrome actions. For coil formation, a radiation similar to A was used. The variation of CPD level versus the wavelengths and fluences of UV-B did not correlate with that of anthocyanin synthesis, but did so with the inhibition of anthocyanin synthesis above a critical level of CPDs. Coil formation was also correlated with CPDs (measured as CTD) above a critical level, which was observed not only when CPD level was raised by increasing the fluence of UV-B, but also when it was lowered by UV-A photorepair. The results supported the view that anthocyanin induction does not involve DNA damage, whereas anthocyanin inhibition may be associated with it. The coil formation was indicated to be caused by it. Pyrimidine (6-4) pyrimidinone photoproducts were formed in proportion to CPDs, and hence, it was impossible to determine which of the two kinds of dimers was responsible. The presence of a fast elimination of CPDs (half-life of ca. 30 min) in the dark was suggested.