The promoter activity of sen1, a senescence-associated gene of Arabidopsis, is repressed by sugars

A senescence-associated gene of Arabidopsis thaliana, sen1, was previously shown to be distinctively regulated by several senescence-inducing factors including dark treatment. In this study, the promoter region of the sen1 gene was fused to the beta-glucuronidase (GUS) reporter gene and introduced into tobacco plants to examine the regulation mechanism of this gene by dark treatment. The sen1 gene expression was highly induced by dark and abscisic acid treatment in transgenic tobacco as in Arabidopsis. The promoter activity was rapidly induced by dark treatment but the values of senescence parameters (chlorophyll content, photochemical efficiency, soluble protein content) changed only slightly during dark incubation for 4 days, showing that dark activation of the sen1 promoter was not closely associated with major symptoms of leaf senescence. 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) treatment of the excised transgenic tobacco leaves in light caused activation of the sen1 promoter and this was concomitant with a decrease in sugar levels, indicating that sugar content may be related to the regulation of the sen1 promoter. Dark-induced activation of the sen1 promoter was highly suppressed by addition of exogenous sucrose at physiological concentrations. Glucose and fructose were also effective in suppressing the activity of the sen1 promoter. However, mannitol or 3-O-methyl-D-glucose, a non-metabolizable analog of glucose did not suppress the promoter activity. We further confirmed that the dark activation of the sen1 promoter was associated with a decrease in sugar content. Our results clearly demonstrate that the promoter of the sen1 gene is negatively regulated by sugar and the dark-induced activation of the sen1 promoter is due to release of the suppression of the sen1 promoter activity by sugar. These data imply that the senescence-associated gene, sen1, is activated upon sugar starvation, recognizing sugar starvation as one of senescence signals.