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Phytochrome Control of Anthocyanin Biosynthesis in Tomato Seedlings: Analysis Using Photomorphogenic Mutants
Authors:L. H. J. Kerckhoffs  M. E. L. Schreuder  A. Van Tuinen  M. Koornneef  R. E. Kendrick
Affiliation:Departments of Plant Physiology, Wageningen Agricultural University, Wageningen, the Netherlands;Departments of Genetics, Wageningen Agricultural University, Wageningen, the Netherlands
Abstract:Anthocyanin biosynthesis has been studied in hypocotyls and whole seedlings of tomato (Lycoperskon esculentum Mill.) wild types (WTs) and photomorphogenic mutants. In white light (WL)/dark (D) cycles the fri1 mutant, deficient in phytochrome A (phyA), shows an enhancement of anthocyanin accumulation, whereas the tri1 mutant, deficient in phytochrome Bl (phyBl) has a WT level of anthocyanin. Under pulses of red light (R) or R followed by far-red light (FR) given every 4 h, phyA is responsible for the non-R/FR reversible response, whereas phyBl is partially responsible for the R/FR reversible response. From R and blue light (B) pretreatment studies, B is most effective in increasing phytochrome responsiveness, whereas under R itself it appears to be dependent on the presence of phyBl. Anthocyanin biosynthesis during a 24 h period of monochromatic irradiation at different flu-ence rates of 4 day-old D-grown seedlings has been studied. At 660 nm the fluence rate-response relationships for induction of anthocyanin in the WT are similar, yet complex, showing a low fluence rate response (LFRR) and a fluence rate-dependent high irradiance response (HIR). The high-pigment-1 (hp-1) mutant exhibits a strong amplification of both the LFRR and HIR. The fri1 mutant lacks the LFRR while retaining a normal HIR. In contrast, a transgenic tomato line overexpressing the oat PHYA3 gene shows a dramatic amplification of the LFRR. The tri1 mutant, retains the LFRR but lacks the HIR, whereas the fri1, tri1 double mutant lacks both components. Only an LFRR is seen at 729 nm in WT; however, an appreciable HIR is observed at 704 nm, which is retained in the tri1 mutant and is absent in the fri1 mutant, indicating the labile phyA pool regulates this response component.
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