期刊
CELL
卷 148, 期 4, 页码 765-779出版社
CELL PRESS
DOI: 10.1016/j.cell.2011.12.024
关键词
-
资金
- NIH [1-R560NS-048471, 2R01NS04847]
Although molecular components of the circadian clock are known, mechanisms that transmit signals from the clock and produce rhythmic behavior are poorly understood. We find that the microRNA miR-279 regulates the JAK/STAT pathway to drive rest: activity rhythms in Drosophila. Overexpression of microRNA miR-279 or miR-279 deletion attenuates rest: activity rhythms. Oscillations of the clock protein PERIOD are normal in pacemaker neurons lacking miR-279, suggesting that miR-279 acts downstream of the clock. We identify the JAK/STAT ligand, Upd, as a target of miR-279 and show that knockdown of Upd rescues the behavioral phenotype of miR-279 mutants. Manipulations of the JAK/STAT pathway also disrupt circadian rhythms. In addition, central clock neurons project in the vicinity of Upd-expressing neurons, providing a possible physical connection by which the central clock could regulate JAK/STAT signaling to control rest: activity rhythms.
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