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Zac1 Regulates Cell Cycle Arrest in Neuronal Progenitors via Tcf4

MPG-Autoren
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Schmidt-Edelkraut,  Udo
Max Planck Institute of Psychiatry, Max Planck Society;

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Daniel,  Guillaume
Max Planck Institute of Psychiatry, Max Planck Society;

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Hoffmann,  Anke
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

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Spengler,  Dietmar
Dept. Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Max Planck Society;

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Zitation

Schmidt-Edelkraut, U., Daniel, G., Hoffmann, A., & Spengler, D. (2014). Zac1 Regulates Cell Cycle Arrest in Neuronal Progenitors via Tcf4. MOLECULAR AND CELLULAR BIOLOGY, 34(6), 1020-1030. doi:10.1128/MCB.01195-13.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0026-A7A4-4
Zusammenfassung
Imprinted genes play a critical role in brain development and mental health, although the underlying molecular and cellular mechanisms remain incompletely understood. The family of basic helix-loop-helix (bHLH) proteins directs the proliferation, differentiation, and specification of distinct neuronal progenitor populations. Here, we identified the bHLH factor gene Tcf4 as a direct target gene of Zac1/Plagl1, a maternally imprinted transcriptional regulator, during early neurogenesis. Zac1 and Tcf4 expression levels concomitantly increased during neuronal progenitor differentiation; moreover, Zac1 interacts with two cis-regulatory elements in the Tcf4 gene locus, and these elements together confer synergistic activation of the Tcf4 gene. Tcf4 up-regulation enhances the expression of the cyclin-dependent kinase inhibitor gene p57(Kip2), a paternally imprinted Tcf4 target gene, and increases the number of cells in G(1) phase. Overall, we show that Zac1 controls cell cycle arrest function in neuronal progenitors through induction of p57Kip2 via Tcf4 and provide evidence for cooperation between imprinted genes and a bHLH factor in early neurodevelopment.