This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Goller, T.
Right arrow Articles by Arnold, H.-H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Goller, T.
Right arrow Articles by Arnold, H.-H.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, November 2008, p. 6819-6827, Vol. 28, No. 22
0270-7306/08/$08.00+0     doi:10.1128/MCB.01058-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Transcriptional Regulator BPTF/FAC1 Is Essential for Trophoblast Differentiation during Early Mouse Development{triangledown}

Tobias Goller,{dagger} Franz Vauti, Suresh Ramasamy, and Hans-Henning Arnold*

Cell and Molecular Biology, University of Braunschweig, Spielmann Strasse 7, 38106 Braunschweig, Germany

Received 7 July 2008/ Accepted 6 September 2008

The putative transcriptional regulator BPTF/FAC1 is expressed in embryonic and extraembryonic tissues of the early mouse conceptus. The extraembryonic trophoblast lineage in mammals is essential to form the fetal part of the placenta and hence for the growth and viability of the embryo in utero. Here, we describe a loss-of-function allele of the BPTF/FAC1 gene that causes embryonic lethality in the mouse. BPTF/FAC1-deficient embryos form apparently normal blastocysts that implant and develop epiblast, visceral endoderm, and extraembryonic ectoderm including trophoblast stem cells. Subsequent development of mutants, however, is arrested at the early gastrula stage (embryonic day 6.5), and virtually all null embryos die before midgestation. Most notably, the ectoplacental cone is drastically reduced or absent in mutants, which may cause the embryonic lethality. Development of the mutant epiblast is also affected, as the anterior visceral endoderm and the primitive streak do not form correctly, while brachyury-expressing mesodermal cells arise but are delayed. The mutant phenotype suggests that gastrulation is initiated, but no complete anteroposterior axis of the epiblast appears. We conclude that BPTF/FAC1 is essential in the extraembryonic lineage for correct development of the ectoplacental cone and fetomaternal interactions. In addition, BPTF/FAC1 may also play a role either directly or indirectly in anterior-posterior patterning of the epiblast.

* Corresponding author. Mailing address: Cell and Molecular Biology, Institute for Biochemistry and Biotechnology, University of Braunschweig, Spielmann Str. 7, 38106 Braunschweig, Germany. Phone: 49 531 3915735. Fax: 49 531 3918178. E-mail: h.arnold{at}tu-bs.de

{triangledown} Published ahead of print on 15 September 2008.

{dagger} Present address: Section Biochemistry II, Center for Biochemistry and Molecular Cell Biology, University of Göttingen, Heinrich Dükerweg 2, 37073 Göttingen, Germany.

Molecular and Cellular Biology, November 2008, p. 6819-6827, Vol. 28, No. 22
0270-7306/08/$08.00+0     doi:10.1128/MCB.01058-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»