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Silencing and un-silencing of tetracycline-controlled genes in neurons

MPG-Autoren
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Bausen,  Melanie
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Herb,  Jan
Max Planck Research Group Behavioural Neurophysiology (Andreas T. Schaefer), Max Planck Institute for Medical Research, Max Planck Society;

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Sawinski,  Jürgen
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

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Cetin,  Ali
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Osten,  Pavel
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Seeburg,  Peter H.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Hasan,  Mazahir T.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;
Department of Biomedical Optics, Max Planck Institute for Medical Research, Max Planck Society;

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Zitation

Zhu, P., Aller, M. I., Baron, U., Cambridge, S., Bausen, M., Herb, J., et al. (2007). Silencing and un-silencing of tetracycline-controlled genes in neurons. PLoS One, 2(6), 1-10. doi:10.1371/journal.pone.0000533.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-002C-AE1B-F
Zusammenfassung
To identify the underlying reason for the controversial performance of tetracycline (Tet)-controlled regulated gene expression in mammalian neurons, we investigated each of the three components that comprise the Tet inducible systems, namely tetracyclines as inducers, tetracycline-transactivator (tTA) and reverse tTA (rtTA), and tTA-responsive promoters (P(tets)). We have discovered that stably integrated P(tet) becomes functionally silenced in the majority of neurons when it is inactive during development. P(tet) silencing can be avoided when it is either not integrated in the genome or stably-integrated with basal activity. Moreover, long-term, high transactivator levels in neurons can often overcome integration-induced P(tet) gene silencing, possibly by inducing promoter accessibility.