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Papers In Press, published online ahead of print December 10, 2001
Dept. of Developmental Pathology, Institute of Pathology, Bonn University, BONN 53127
Corresponding Author: hubert.schorle{at}ukb.uni-bonn.de
The transcription factor AP-2
J. Biol. Chem, 10.1074/jbc.M108578200
Submitted on September 6, 2001
Revised on December 10, 2001
Accepted on December 10, 2001
A subtractive gene expression screen suggests a role of transcription factor AP-2alpha in control of proliferation and differentiation
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-2 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 in E 8 - 9 mouse embryos. Homozygous AP-2 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. Using a subtractive cloning approach we identified a set of genes repressed by AP-2 which are described to retard cellular proliferation and induce differentiation and apoptosis. We show that these target genes are prematurely expressed in AP-2 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-2 display retarded growth but no enhanced apoptosis. Based on these data we suggest that AP-2 might be required for cell proliferation by suppression of genes inducing terminal differentiation apoptosis and growth retardation.
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