There is increasing evidence that disruption of the circadian clock in metabolic organs plays a key role in pathologies such as obesity or diabetes. To clarify the mechanisms involved, we have designed a mathematical model of the mammalian liver clock synchronized to feeding/fasting cycles via the intracellular factors NAD+ and AMP (Woller et al, Cell Rep 17, 1087, 2016). We seek a PhD student to develop biophotonic experiments with cell cultures to obtain data for validating and extending this model. Using reporters and biosensors for key metabolic actors such as SIRT1 or AMPK, as well as for core clock genes, we will quantify how various factors reset the circadian clock of hepatocytes and compare measurements with model predictions, but also validate molecular interactions playing a central role in the model.