Persistent epigenetic reprogramming of sweet taste by diet.

Persistent epigenetic reprogramming of sweet taste by diet.
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DOI:
10.1126/sciadv.abc8492
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发表时间:
2020-11
期刊:
影响因子:
13.6
通讯作者:
Dus M
Dus M
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Vaziri A;Khabiri M;Genaw BT;May CE;Freddolino PL;Dus M

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Diets high in sugar persistently alter sensory responses to sweetness through the actions of the PRC2 complex to promote obesity. Diets rich in sugar, salt, and fat alter taste perception and food preference, 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 epigenetic regulator Polycomb Repressive Complex 2.1 (PRC2.1) persistently reprograms the sensory neurons of Drosophila melanogaster flies to reduce sweet sensation and promote obesity. In animals fed high sugar, the binding of PRC2.1 to the chromatin of the sweet gustatory neurons is redistributed to repress a developmental transcriptional network that modulates the responsiveness of these cells to sweet stimuli, reducing sweet sensation. Half of these transcriptional changes persist despite returning the animals to a control diet, causing a permanent decrease in sweet taste. Our results uncover a new epigenetic mechanism that, in response to the dietary environment, regulates neural plasticity and feeding behavior to promote obesity.
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