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Miz1 Is Required for Early Embryonic Development during Gastrulation

Sovana Adhikary,¹ Karen Peukert,¹ Holger Karsunky,^2, Vincent Beuger,¹ Werner Lutz,¹ Hans-Peter Elsässer,³ Tarik Möröy,² and Martin Eilers^1*

Institute for Molecular Biology and Tumor Research,¹ Institute for Cytobiology and Cytopathology, University of Marburg, 35033 Marburg,³ Institute for Cell Biology, Universitätsklinikum Essen, 45122 Essen, Germany²

Received 4 April 2003/ Returned for modification 15 May 2003/ Accepted 23 July 2003

Miz1 is a member of the POZ domain/zinc finger transcription factor family. In vivo, Miz1 forms a complex with the Myc oncoprotein and recruits Myc to core promoter elements. Myc represses transcription through Miz1 binding sites. We now show that the Miz1 gene is ubiquitously expressed during mouse embryogenesis. In order to elucidate the physiological function of Miz1, we have deleted the mouse Miz1 gene by homologous recombination. Miz1^+/- mice are indistinguishable from wild-type animals; in contrast, Miz1^-/- embryos are not viable. They are severely retarded in early embryonic development and do not undergo normal gastrulation. Expression of Goosecoid and Brachyury is detectable in Miz1^-/- embryos, suggesting that Miz1 is not required for signal transduction by Nodal. Expression of p21Cip1, a target gene of Miz1 is unaltered; in contrast, expression of p57Kip2, another target gene of Miz1 is absent in Miz1^-/- embryos. Miz1^-/- embryos succumb to massive apoptosis of ectodermal cells around day 7.5 of embryonic development. Our results show that Miz1 is required for early embryonic development during gastrulation.

Present address: Department of Pathology, Stanford University, Stanford, CA 94305.

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