Abstract

Broad‐band UV‐B radiation inhibited hypocotyl elongation in etiolated tomato (Lycopersicon esculentum Mill. cv. Alisa Craig) seedlings. This inhibition could be elicited by < 3 μmol m−2 s−1 of UV‐B radiation provided against a background of white light (> 620 μmol m−2 s−1 between 320 and 800 nm), and was similar in wild‐type and phytochrome‐1‐deficient aurea mutant seedlings. These observations suggest that the effect of UV‐B radiation is not mediated by phytochrome. An activity spectrum obtained by delivering 1 μmol m−2 s−1 of monochromatic UV radiation against a while light background (63 μmol m−2 s−1 showed maximum effectiveness around 300 nm, which suggests that DNA or aromatic residues in proteins are not the chromophores mediating UV‐B induced inhibition of elongation. Chemicals that affect the normal (photo)chemistry of flavins and possibly pterins (KI, NaN, and phenylacetic acid) largely abolished the inhibitor) effect of broad‐hand UV‐B radiation when applied to the root zone before irradiation. KI was effective at concentrations < 10−4M, which have been shown in vitro to be effective in quenching the triplet excited stales of flavins but not fluorescence from pterine or singlet states of flavins. Elimination of blue light or reduction of UV‐A, two sources of flavin excitation, promoted hypocotyl elongation, but did not affect the inhibition of elongation evened by UV‐B. Kl applied after UV‐B irradiation had no effect on the inhibition response. Taken together these findings suggest that the chromophore of the photoreceptor system invoked in UV‐B perception by tomato seedlings during de‐etiolation may be a flavin.

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