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Published 3 January 2006. doi:10.1083/jcb.200506057
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 172, Number 1, 139-149
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Article

 Myc regulates keratinocyte adhesion and differentiation via complex formation with Miz1

Anneli Gebhardt1, Michaela Frye3, Steffi Herold2, Salvador Aznar Benitah3, Kristin Braun3, Birgit Samans2, Fiona M. Watt3, Hans-Peter Elsässer1, and Martin Eilers2

1 Institute for Cell Biology, University of Marburg, 35033 Marburg, Germany
2 Institute for Molecular Biology and Tumor Research, University of Marburg, 35033 Marburg, Germany
3 Cancer Research UK London Research Institute, London WC2A 3PX, England, UK

Correspondence to Martin Eilers: eilers{at}imt.uni-marburg.de

Myc plays a key role in homeostasis of the skin. We show that Miz1, which mediates Myc repression of gene expression, is expressed in the epidermal basal layer. A large percentage of genes regulated by the Myc–Miz1 complex in keratinocytes encode proteins involved in cell adhesion, and some, including the {alpha}6 and ß1 integrins, are directly bound by Myc and Miz1 in vivo. Using a Myc mutant deficient in Miz1 binding (MycV394D), we show that Miz1 is required for the effects of Myc on keratinocyte responsiveness to TGF-ß. Myc, but not MycV394D, decreases keratinocyte adhesion and spreading. In reconstituted epidermis, Myc induces differentiation and loss of cell polarization in a Miz1-dependent manner. In vivo, overexpression of ß1 integrins restores basal layer polarity and prevents Myc-induced premature differentiation. Our data show that regulation of cell adhesion is a major function of the Myc–Miz1 complex and suggest that it may contribute to Myc-induced exit from the epidermal stem cell compartment.

A. Gebhardt and M. Frye contributed equally to this paper.

Abbreviations used in this paper: 4-OHT, 4-hydroxy-tamoxifen; cDNA, complementary DNA; ChIP, chromatin immunoprecipitation; DED, de-epidermized dermis.


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