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Journal Article

TfAP-2 is required for night sleep in Drosophila.

MPS-Authors
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Kucherenko,  M. M.
Research Group of Gene Expression and Signaling, MPI for biophysical chemistry, Max Planck Society;

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Ilangovan,  V.
Department of Genes and Behavior, MPI for Biophysical Chemistry, Max Planck Society;

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Shcherbata,  H. R.
Research Group of Gene Expression and Signaling, MPI for biophysical chemistry, Max Planck Society;

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Bringmann,  H.
Research Group of Sleep and Waking, MPI for biophysical chemistry, Max Planck Society;

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2359103_Suppl.docx
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Citation

Kucherenko, M. M., Ilangovan, V., Herzig, Shcherbata, H. R., & Bringmann, H. (2016). TfAP-2 is required for night sleep in Drosophila. BMC Neuroscience, 17: 72. doi:10.1186/s12868-016-0306-3.


Cite as: https://hdl.handle.net/11858/00-001M-0000-002B-B97A-8
Abstract
BACKGROUND: The 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. RESULTS: Drosophila 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. CONCLUSIONS: Thus, our results show that AP-2 transcription factors are highly conserved regulators of development and sleep.