LIGHT-INTENSITY REGULATION OF CAB GENE-TRANSCRIPTION IS SIGNALED BY THE REDOX STATE OF THE PLASTOQUINONE POOL

The eukaryotic green alga Dunaliella tertiolecta acclimates to decreas ed growth irradiance by increasing cellular levels of light-harvesting chlorophyll protein complex apoproteins associated with photosystem I I (LHCIIs), whereas increased growth irradiance elicits the opposite r esponse. Nuclear run-on transcription assays and measurements of cab m RNA stability established that light intensity-dependent changes in LH CII are controlled at the level of transcription, cab gene transcripti on in high-intensity light was partially enhanced by reducing plastoqu inone with 3-(3,4-dichlorophenyl)-1,1-dimethyl urea (DCMU), whereas it was repressed in low-intensity light by partially inhibiting the oxid ation of plastoquinol with 2,5-dibromo-3-methyl-6-isopropyl-p-benzoqui none (DBMIB). Uncouplers of photosynthetic electron transport and inhi bition of water splitting had no effect on LHCII levels. These results strongly implicate the redox state of the plastoquinone pool in the c hloroplast as a photon-sensing system that is coupled to the light-int ensity regulation of nuclear-encoded cab gene transcription. The accum ulation of cellular chlorophyll at low-intensity light can be blocked with cytoplasmically directed phosphatase inhibitors, such as okadaic acid, microcystin L-R, and tautomycin. Gel mobility-shift assays revea led that cells grown in high-intensity light contained proteins that b ind to the promoter region of a cab gene carrying sequences homologous to higher plant light-responsive elements. On the basis of these expe rimental results, we propose a model for a light intensity signaling s ystem where cab gene expression is reversibly repressed by a phosphory lated factor coupled to the redox status of plastoquinone through a ch loroplast protein kinase.