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Vol. 12, No. 8, pp. 1227-1239, April 15, 1998
1 Laboratory for Molecular Carcinogenesis, Sylvius
Laboratories, University of Leiden, 2300 RA Leiden, The Netherlands;
2 Forschungszentrum Karlsruhe, Institute of Genetics, 76021 Karlsruhe, Germany;
3 Unité de Virologie Humaine,
Institut National de la Santé et de la Recherche Médicale
(INSERM)-U412, Ecole Normale Supérieure, Lyon Cedex 07, France;
4 Department of Signal Transduction and Growth Control,
Deutsches Krebsforschungszentrum, Heidelberg, Germany
Cellular transformation can be achieved by constitutive activation
of growth-regulatory signaling pathways, which, in turn, activate
nuclear transcription factors thought to execute a
transformation-specific program of gene expression. Members of the
dimeric transcription factor family AP-1 are at the receiving end of
such growth-regulating pathways and the viral form of the AP-1 subunit
Jun establishes one important aspect of transformation in chick embryo
fibroblasts (CEFs): enhanced growth in agar and in low serum. Enhanced
Jun activity is likely to target several different genetic programs as
Jun forms heterodimers with one of several members of the Fos and ATF2
subfamilies, resulting in transcription factors with different sequence
specificities. To identify the programs relevant for transformation, we
have reduced the complexity of AP-1 factors by constructing Jun bZip
mutants that can efficiently dimerize and transactivate with only a
restricted set of partner subunits. Upon introduction into CEFs, a Jun
mutant selective for the Fos family induced anchorage-independent
growth but no growth factor-independence. In contrast, a c-Jun mutant
with preference for ATF2-like proteins caused growth
factor-independence, but no growth in agar. Coexpression of both
mutants reestablished the combined transformation program as induced by
wild-type Jun. These data show that Jun-dependent cell transformation
can be resolved into at least two distinct and independent processes,
anchorage and growth factor independence, obviously triggered by two
classes of Jun heterodimers likely regulating different sets of target genes.
[Key Words: ATF2; Fos; bZip mutants; transcription; transformation; chick embryo fibroblasts; anchorage independence; growth factor independence]
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