Genetic and Developmental Control of Nuclear Accumulation of COPI , a Repressor of Photomorphogenesis in Arabidopsis ’

Using a P-glucuronidase (CUS) reporter-COPl fusion transgene, it was shown previously that Arabidopsis COPl acts within the nucleus as a repressor of seedling photomorphogenic development and that light inactivation of COPl was accompanied by a reduction of COPl nuclear abundance (A.C. von Arnim, X.-W. Deng [I9941 Cell 79: 1035-1045). Here we report that the GUS-COPl fusion transgene can completely rescue the defect of cop l mutations and thus is fully functional during seedling development. l h e kinetics of CUS-COPI relocalization in a cop l null mutant background during dark/light transitions imply that the regulation of the functional nuclear COPl level plays a role in stably maintaining a committed seedling’s developmental fate rather than in causing such a commitment. Analysis of GUS-COP1 cellular localization in mutant hypocotyls of all other pleiotropic COP/DET/FUS loci revealed that nuclear localization of CUS-COP1 was diminished under both dark and light conditions in all mutants tested, whereas nuclear localization was not affected in the less pleiotropic cop4 mutant. Using both the brassinosteroid-deficient mutant detZ and brassinosteroid treatment of wild-type seedlings, we have demonstrated that brassinosteroid does not control the hypocotyl cell elongation through regulating nuclear localization of COPl . l h e growth regulator cytokinin, which also dramatically reduced hypocotyl cell elongation in the absence of light, did not prevent CUSCOPl nuclear localization in dark-grown seedlings. Our results suggest that all of the previously characterized pleiotropic COP/ DE7/FUS loci are required for the proper nuclear localization of the COPl protein in the dark, whereas the less pleiotropic COP/DET loci or plant regulators tested are likely to act either downstream of COPl or by independent pathways.