Persistent epigenetic reprogramming of sweet taste for a high-sugar diet
Diets rich in sugar, salt and fat alter the perception of taste and preference for food, contributing to obesity and metabolic disorders, but the molecular mechanisms through which this occurs are unknown. Here, we show that in response to a high-sugar diet, the Polycomb Repressive Complex 2.1 epigenetic regulator (PRC2.1) persistently reprograms sensory neurons from Drosophila melanogaster flies to reduce sweet feeling and promote obesity. In high-sugar-fed animals, the binding of PRC2.1 to the chromatin of sweet taste neurons is redistributed to suppress a transcriptional developmental network that modulates the responsiveness of these cells to sweet stimuli, reducing sweet sensation. Half of these transcriptional changes persist even though the animals return to a control diet, leading to a permanent decrease in sweet taste. Our results discover a new epigenetic mechanism that, in response to the dietary environment, regulates neural plasticity and food behavior to promote obesity.
