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Originally published In Press as doi:10.1074/jbc.M108578200 on December 10, 2001

J. Biol. Chem., Vol. 277, Issue 8, 6637-6644, February 22, 2002
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A Subtractive Gene Expression Screen Suggests a Role of Transcription Factor AP-2alpha in Control of Proliferation and Differentiation*

Petra PfistererDagger , Julia Ehlermann§, Martin HegenDagger , and Hubert SchorleDagger §

From the Dagger  Forschungszentrum Karlsruhe, ITG, Hermann von Helmholtz Platz 1, 76344 Eggenstein-Leopoldshafen and the § Department of Developmental Pathology, Institute of Pathology, Bonn University, Sigmund-Freud Strasse 25, 53127 Bonn, Germany

The transcription factor AP-2alpha has been implicated as a cell type-specific regulator of gene expression during vertebrate embryogenesis based on its expression pattern in neural crest cells, ectoderm, and the nervous system in mouse and frog embryos. AP-2alpha is prominently expressed in cranial neural crest cells, a population of cells that migrate from the lateral margins of the brain plate during closure of the neural tube at day 8-9 of embryonic development. Homozygous AP-2alpha mutant mice die perinatally with cranio-abdominoschisis, full facial clefting, and defects in cranial ganglia and sensory organs, indicating the importance of this gene for proper development. By using a subtractive cloning approach, we identified a set of genes repressed by AP-2alpha that are described to retard cellular proliferation and induce differentiation and apoptosis. We show that these target genes are prematurely expressed in AP-2alpha mutant mice. One of the genes isolated, the Krüppel-box transcription factor KLF-4 implicated in induction of terminal differentiation and growth regulation, is found expressed in mutant embryonic fibroblasts. We show that fibroblasts lacking AP-2alpha display retarded growth but no enhanced apoptosis. Based on these data we suggest that AP-2alpha might be required for cell proliferation by suppression of genes inducing terminal differentiation, apoptosis, and growth retardation.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Supported by Deutsche Forschungsgemeinschaft Grant 503/2. To whom correspondence should be addressed: Dept. of Developmental Pathology, Institute of Pathology, Bonn University, Sigmund-Freud Strasse 25, 53127 Bonn, Germany. Tel.: 49-228-287-6342; Fax: 49-228-287-5030; E-mail: Hubert.Schorle@ukb.uni-bonn.de.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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