TfAP-2 is required for night sleep in Drosophila

BMC Neuroscience

Research Article

Vinodh Ilangovan¹  Halyna R. Shcherbata²  Mariya M. Kucherenko²  Bettina Herzig³  Henrik Bringmann³ 

[1] Department of Genes and Behavior, Max Planck Institute for Biophysical Chemistry, Göttingen, Germany;Max Planck Research Group Gene Expression and Signaling, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077, Göttingen, Germany;Max Planck Research Group Sleep and Waking, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077, Göttingen, Germany;

关键词: Drosophila;    AP-2;    Char syndrome;    Insomnia;    C. elegans;   

DOI  :  10.1186/s12868-016-0306-3

 received in 2016-04-19, accepted in 2016-10-31,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundThe AP-2 transcription factor APTF-1 is crucially required for developmentally controlled sleep behavior in Caenorhabditis elegans larvae. Its human ortholog, TFAP-2beta, causes Char disease and has also been linked to sleep disorders. These data suggest that AP-2 transcription factors may be highly conserved regulators of various types of sleep behavior. Here, we tested the idea that AP-2 controls adult sleep in Drosophila.ResultsDrosophila has one AP-2 ortholog called TfAP-2, which is essential for viability. To investigate its potential role in sleep behavior and neural development, we specifically downregulated TfAP-2 in the nervous system. We found that neuronal TfAP-2 knockdown almost completely abolished night sleep but did not affect day sleep. TfAP-2 insufficiency affected nervous system development. Conditional TfAP-2 knockdown in the adult also produced a modest sleep phenotype, suggesting that TfAP-2 acts both in larval as well as in differentiated neurons.ConclusionsThus, our results show that AP-2 transcription factors are highly conserved regulators of development and sleep.

【 授权许可】

CC BY   
© The Author(s) 2016

【 图 表 】

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