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Development 129, 2733-2747 (2002)
© 2002 The Company of Biologists Limited

Transcription factor AP-2{gamma} is essential in the extra-embryonic lineages for early postimplantation development

Heidi J. Auman1, Timothy Nottoli1,*, Olga Lakiza1,{dagger}, Quinton Winger2, Stephanie Donaldson1 and Trevor Williams1,2,{ddagger}

1 Department of Molecular, Cellular and Developmental Biology, Yale University, 266 Whitney Avenue, New Haven, CT 06511, USA
2 Departments of Craniofacial Biology, and Cellular and Structural Biology, BRB151, Campus Box C286, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Denver, CO 80262, USA
* Present address: Gene Targeting Service, Section of Comparative Medicine, Yale University School of Medicine, PO Box 208016, New Haven, CT 06520-8016, USA
{dagger} Present address: Northwestern University Medical School, Children’s Memorial Hospital, 2300 Children’s Plaza, MC 204, Chicago, IL 60614, USA

{ddagger}Author for correspondence (e-mail: trevor.williams{at}uchsc.edu)

Accepted 14 March 2002

The members of the AP-2 family of transcription factors play important roles during mammalian development and morphogenesis. AP-2{gamma} (Tcfap2c – Mouse Genome Informatics) is a retinoic acid-responsive gene implicated in placental development and the progression of human breast cancer. We show that AP-2{gamma} is present in all cells of preimplantation embryos and becomes restricted to the extra-embryonic lineages at the time of implantation. To study further the biological function of AP-2{gamma}, we have generated Tcfap2c-deficient mice by gene disruption. The majority of Tcfap2c–/– mice failed to survive beyond 8.5 days post coitum (d.p.c.). At 7.5 d.p.c., Tcfap2c–/– mutants were typically arrested or retarded in their embryonic development in comparison to controls. Morphological and molecular analyses of mutants revealed that gastrulation could be initiated and that anterior-posterior patterning of the epiblast remained intact. However, the Tcfap2c mutants failed to establish a normal maternal-embryonic interface, and the extra-embryonic tissues were malformed. Moreover, the trophoblast-specific expression of eomesodermin and Cdx2, two genes implicated in FGF-responsive trophoblast stem cell maintenance, was significantly reduced. Chimera studies demonstrated that AP-2{gamma} plays no major autonomous role in the development of the embryo proper. By contrast, the presence of AP-2{gamma} in the extra-embryonic membranes is required for normal development of this compartment and also for survival of the mouse embryo.

Key words: Tcfap2c mutant mouse, Postimplantation development, Extra-embryonic, Trophoblast, AP-2{gamma}




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© The Company of Biologists Ltd 2002