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c-Jun is essential for normal mouse development and hepatogenesis

Nature volume 365, pages 179–181 (1993)Cite this article

An Erratum to this article was published on 25 December 1993

Abstract

THE proto-oncogene c-jun is the cellular homologue of v-jun, the transforming oncogene of the avian sarcoma virus 17 (ref. 1). c-jun encodes one major component of the AP-1 transcription fac-tor complex and is expressed in many organs during mouse development and in the adult2–4. Because of its rapid induction in cells following growth stimulation and the presence of AP-1 binding sites in the promoter regions of many genes, the c-Jun protein is thought to have important functions in cell proliferation and differentiation2,5–10. But embryonic stem (ES) cells lacking c-Jun are viable and have a normal in vitro differentiation capacity, although c-Jun appears to be important for growth of teratocarcinomas in vivo11. To define the function of c-jun better, targeted ES cells were used to generate mice lacking c-Jun. Here we report that heterozygous mutant mice appear normal, but embryos lacking c-Jun die at mid- to late-gestation and exhibit impaired hepatogenesis, altered fetal liver erythropoiesis and generalized oedema. Interestingly, c-jun-/- ES cells can

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Author notes

  1. Frank Hilberg

    Present address: Bender & Co. Ges.m.b.H., Dr Boehringer-Gasse 5, A-1120, Vienna, Austria

  2. Adriano Aguzzi: Institute of Neuropathology, Schmelzbergstrasse 12, CH-8091 Zurich, Switzerland

Authors and Affiliations

  1. Research Institute of Molecular Pathology (IMP), Dr Bohr-Gasse 7, A-1030, Vienna, Austria

    Frank Hilberg, Adriano Aguzzi, Norma Howells & Erwin F. Wagner

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  1. Frank Hilberg
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  4. Erwin F. Wagner
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Hilberg, F., Aguzzi, A., Howells, N. et al. c-Jun is essential for normal mouse development and hepatogenesis. Nature 365, 179–181 (1993). https://doi.org/10.1038/365179a0

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