Journal
BMC NEUROSCIENCE
Volume 17, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s12868-016-0306-3
Keywords
Drosophila; AP-2; Char syndrome; Insomnia; C. elegans
Categories
Funding
- Max Planck Society
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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.
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