Suppressor of Overexpression of CO 1 Negatively Regulates Dark-Induced Leaf Degreening and Senescence by Directly Repressing Pheophytinase and Other Senescence-Associated Genes in Arabidopsis.

Although the biochemical pathway of chlorophyll (Chl) degradation has been largely elucidated, how Chl is rapidly yet coordinately degraded during leaf senescence remains elusive. Pheophytinase (PPH) is the enzyme for catalyzing the removal of the phytol group from pheophytin , and expression is significantly induced during leaf senescence. To elucidate the transcriptional regulation of , we used a yeast () one-hybrid system to screen for its trans-regulators. SUPPRESSOR OF OVEREXPRESSION OF CO 1 (SOC1), a key flowering pathway integrator, was initially identified as one of the putative trans-regulators of After dark treatment, leaves of an knockdown mutant () showed an accelerated yellowing phenotype, whereas those of -overexpressing lines exhibited a partial stay-green phenotype. and expression showed a negative correlation during leaf senescence. Substantially, SOC1 protein could bind specifically to the CArG box of the promoter in vitro and in vivo, and overexpression of significantly inhibited the transcriptional activity of the promoter in Arabidopsis () protoplasts. Importantly, (a knockout mutant) double mutant displayed a stay-green phenotype similar to that of during dark treatment. These results demonstrated that SOC1 inhibits Chl degradation via negatively regulating expression. In addition, measurement of the Chl content and the maximum photochemical efficiency of photosystem II of and leaves after dark treatment suggested that SOC1 also negatively regulates the general senescence process. Seven () were thereafter identified as its potential target genes, and and were experimentally confirmed. Together, we reveal that SOC1 represses dark-induced leaf Chl degradation and senescence in general in Arabidopsis.