Myocardial contractile dysfunction is associated with an increase in mitochondrial fission in patients with diabetes. However, whether mitochondrial fission directly promotes diabetes‐induced cardiac dysfunction is still unknown. Melatonin exerts a substantial influence on the regulation of mitochondrial fission/fusion. This study investigated whether melatonin protects against diabetes‐induced cardiac dysfunction via regulation of mitochondrial fission/fusion and explored its underlying mechanisms. Here, we show that melatonin prevented diabetes‐induced cardiac dysfunction by inhibiting dynamin‐related protein 1 (Drp1)‐mediated mitochondrial fission. Melatonin treatment decreased Drp1 expression, inhibited mitochondrial fragmentation, suppressed oxidative stress, reduced cardiomyocyte apoptosis, improved mitochondrial function and cardiac function in streptozotocin (STZ)‐induced diabetic mice, but not in SIRT1−/− diabetic mice. In high glucose‐exposed H9c2 cells, melatonin treatment increased the expression of SIRT1 and PGC‐1α and inhibited Drp1‐mediated mitochondrial fission and mitochondria‐derived superoxide production. In contrast, SIRT1 or PGC‐1α siRNA knockdown blunted the inhibitory effects of melatonin on Drp1 expression and mitochondrial fission. These data indicated that melatonin exerted its cardioprotective effects by reducing Drp1‐mediated mitochondrial fission in a SIRT1/PGC‐1α‐dependent manner. Moreover, chromatin immunoprecipitation analysis revealed that PGC‐1α directly regulated the expression of Drp1 by binding to its promoter. Inhibition of mitochondrial fission with Drp1 inhibitor mdivi‐1 suppressed oxidative stress, alleviated mitochondrial dysfunction and cardiac dysfunction in diabetic mice. These findings show that melatonin attenuates the development of diabetes‐induced cardiac dysfunction by preventing mitochondrial fission through SIRT1‐PGC1α pathway, which negatively regulates the expression of Drp1 directly. Inhibition of mitochondrial fission may be a potential target for delaying cardiac complications in patients with diabetes.

Summary• Glucosinolates are a major class of secondary metabolites found in the Brassicaceae, whose degradation products are proving to be increasingly important for human health and in crop protection.• The genetic and metabolic basis of glucosinolate accumulation was dissected through analysis of total glucosinolate concentration and its individual components in both leaves and seeds of a doubled-haploid (DH) mapping population of oilseed rape ⁄ canola (Brassica napus).• The quantitative trait loci (QTL) that had an effect on glucosinolate concentration in either or both of the organs were integrated, resulting in 105 metabolite QTL (mQTL). Pairwise correlations between individual glucosinolates and prior knowledge of the metabolic pathways involved in the biosynthesis of different glucosinolates allowed us to predict the function of genes underlying the mQTL. Moreover, this information allowed us to construct an advanced metabolic network and associated epistatic interactions responsible for the glucosinolate composition in both leaves and seeds of B. napus.• A number of previously unknown potential regulatory relationships involved in glucosinolate synthesis were identified and this study illustrates how genetic variation can affect a biochemical pathway.

Phosphorus (P) deficiency in soils is a major limiting factor for crop growth worldwide. Changes in root morphology and architecture represent as an important mechanism of adaptation of plants to low P (LP) stress. To elucidate the genetic control of tolerance to P deficiency in Brassica napus, quantitative trait loci (QTL) for root morphology in response to LP were identified in three independent paper culture experiments, and dissected through QTL meta-analysis. In total, 62 significant QTL for total root length, root surface area, root volume, total dry weight, and plant P uptake under high and low P conditions were detected in the three experiments. Forty-five of these QTL were clustered within four linkage groups and were integrated into eight unique QTL by two rounds of QTL meta-analysis. Three of the unique QTL, uq.A1, uq.C3a and uq.C3b, were specific for LP condition. uq.C3a and uq.C3b were identified specifically for root traits and P uptake under LP stress, and may contribute to the adaptability of B. napus to P deficiency. Two functional markers, BnIPS2-C3 and BnGPT1-C3, which were developed from the genes AtIPS2 and AtGPT1 in Arabidopsis, were located in the confidence intervals of uq.C3a and uq.C3b, respectively. And AtGPT1 that corresponded to the interval of uq.C3b by in silico mapping was a possible candidate gene of uq.C3b. These results confirmed the importance of root traits for the adaptability of B. napus to LP and partially revealed the genetic basis of tolerance to P deficiency. These findings should be valuable for further study of the mechanism of P efficiency and the breeding of P-efficient cultivars by marker-assisted selection.

). † These authors contributed equally to this work. SUMMARYThe RPW8 locus from Arabidopsis thaliana Ms-0 includes two functional paralogous genes (RPW8.1 and RPW8.2) and confers broad-spectrum resistance via the salicylic acid-dependent signaling pathway to the biotrophic fungal pathogens Golovinomyces spp. that cause powdery mildew diseases on multiple plant species. To identify proteins involved in regulation of the RPW8 protein function, a yeast two-hybrid screen was performed using RPW8.2 as bait. The 14-3-3 isoform lambda (designated GF14k) was identified as a potential RPW8.2 interactor. The RPW8.2-GF14k interaction was specific and engaged the C-terminal domain of RPW8.2, which was confirmed by pulldown assays. The physiological impact of the interaction was revealed by knocking down GF14k by T-DNA insertion, which compromised basal and RPW8-mediated resistance to powdery mildew. In addition, over-expression of GF14k resulted in hypersensitive response-like cell death and enhanced resistance to powdery mildew via the salicylic acid-dependent signaling pathway. The results from this study suggest that GF14k may positively regulate the RPW8.2 resistance function and play a role in enhancing basal resistance in Arabidopsis.