Anthocyanins are important plant pigments that fulfil many physiological and ecological functions. Anthocyanin biosynthesis is controlled by numerous regulatory factors at the transcriptional level. Jasmonates (JAs) has been shown to induce anthocyanin accumulation in several plant species, however, the molecular mechanism for JA-regulated anthocyanin accumulation remains unknown. In this study, genetic, molecular, and physiological approaches were used to reveal the molecular basis of JA-regulated pigmentation in Arabidopsis. It was found that the F-box protein COI1 was required for JA-specific induced expression of the 'late' anthocyanin biosynthetic genes DFR, LDOX, and UF3GT. It is further demonstrated that COI1 was essential for JA-induction of transcription factors PAP1, PAP2, and GL3. It is speculated that COI1 regulates the expression of the transcription factors, including PAP1, PAP2, and GL3, which mediates the 'late' anthocyanin biosynthetic genes DFR, LDOX, and UF3GT, thereby modulating JA-induced anthocyanin biosynthesis in Arabidopsis.

Leaf senescence, as the last stage of leaf development, is regulated by diverse developmental and environmental factors. Jasmonates (JAs) have been shown to induce leaf senescence in several plant species; however, the molecular mechanism for JA-induced leaf senescence remains unknown. In this study, proteomic, genetic, and physiological approaches were used to reveal the molecular basis of JA-induced leaf senescence in Arabidopsis (Arabidopsis thaliana). We identified 35 coronatineinsensitive 1 (COI1)-dependent JA-regulated proteins using two-dimensional difference gel electrophoresis in Arabidopsis. Among these 35 proteins, Rubisco activase (RCA) was a COI1-dependent JA-repressed protein. We found that RCA was downregulated at the levels of transcript and protein abundance by JA in a COI1-dependent manner. We further found that loss of RCA led to typical senescence-associated features and that the COI1-dependent JA repression of RCA played an important role in JA-induced leaf senescence.

We seek to observe the association between childhood obesity by different measures and adult obesity, metabolic syndrome (MetS), and diabetes. Thousand two hundred and nine subjects from "Beijing Blood Pressure Cohort Study" were followed 22.9 ± 0.5 years in average from childhood to adulthood. We defined childhood obesity using body mass index (BMI) or left subscapular skinfold (LSSF), and adult obesity as BMI ≥ 28 kg/m(2). MetS was defined according to the joint statement of International Diabetes Federation and American Heart Association with modified waist circumference (≥ 90/85 cm for men/women). Diabetes was defined as fasting plasma glucose ≥ 7.0 mmol/L or blood glucose 2 h after oral glucose tolerance test ≥ 11.1 mmol/L or currently using blood glucose-lowering agents. Multiple linear and logistic regression models were used to assess the association. The incidence of adult obesity was 13.4, 60.0, 48.3, and 65.1 % for children without obesity, having obesity by BMI only, by LSSF only, and by both, respectively. Compared to children without obesity, children obese by LSSF only or by both had higher risk of diabetes. After controlling for adult obesity, childhood obesity predicted independently long-term risks of diabetes (odds ratio 2.8, 95 % confidence interval 1.2-6.3) or abdominal obesity (2.7, 1.6-4.7) other than MetS as a whole (1.2, 0.6-2.4). Childhood obesity predicts long-term risk of adult diabetes, and the effect is independent of adult obesity. LSSF is better than BMI in predicting adult diabetes.