Microgrids using renewable energy sources play an important role in providing universal electricity access in rural areas in the Global South. Current methods of system dimensioning rely on stochastic load profile modeling, which has limitations in microgrids with industrial consumers due to high demand side uncertainties. In this paper, we propose an alternative approach considering demand side management during system design which we implemented using a genetic scheduling algorithm. The developed method is applied to a test case system on Idjwi Island, Democratic Republic of the Congo (DRC), which is to be powered by a micro hydropower plant (MHP) in combination with a photovoltaic (PV) system and a battery energy storage system (BESS). The results show that the increased flexibility of industrial consumers can significantly reduce the cost of electricity. Most importantly, the presented method quantifies the trade-off between electricity cost and consumer flexibility. This gives local stakeholders the ability to make an informed compromise and design an off-grid system that covers their electricity needs in the most cost-efficient way.

The coupling between sugar availability and shoot branching is well established, yet the underlying molecular mechanisms remain largely unknown. Here, using genome-wide profiling, we characterized the sugar signalling pathways by identifying 10 miRNAs repressed by glycolysis, the tricarboxylic acid (TCA) cycle, and/or the oxidative pentose phosphate pathway (OPPP) in rose buds. Focusing on RhmiR319, a miRNA repressed under active sugar metabolism, we demonstrate that disruption of both glycolysis/the TCA cycle and the OPPP induces the RhmiR319 accumulation, leading to the concomitant repression of its targets, RhTCP4a and RhTCP4b. We additionally reveal that the miR319/TCP4 module regulates shoot branching in Arabidopsis, as miR319 overexpression impairs shoot branching, whereas TCP4 promotes it. Altered branching patterns in Rose and Arabidopsis were associated with the expression of the branching integrator BRC1. Finally, we provide molecular evidence supporting that RhTCP4a/b directly binds to the RhBRC1 promoter and represses its transcription. Together, these results establish the miR319-TCP4-BRC1 regulatory module as a key component in the regulation of shoot branching in response to sugar status. We propose that the miR319-TCP4-BRC1 module is conserved between annual and perennial species and may integrate multiple hormonal and metabolic signals to shape shoot branching in plants.