|
|||||
|
|
PBX1 is dispensable for neural commitment of RA-treated murine ES cells |
|
| Authors: | Anne S. Jürgens Mateusz Kolanczyk Dietrich C. C. Moebest Tomasz Zemojtel Urs Lichtenauer Marlena Duchniewicz Melanie P. Gantert Jochen Hecht Uwe Hattenhorst Stefan Burdach Annette Dorn Mark P. Kamps Felix Beuschlein Daniel Räpple Jürgen S. Scheele |
| Affiliation: | 1. Department of Medicine I, University of Freiburg Medical Center, Hugstetter Str. 55, 79106, Freiburg, Germany 4. Department of Biology III, Institute for Biology, University of Freiburg, Sch?nzlestr. 1, 79104, Freiburg, Germany 7. Development and Disease Group, Max-Planck-Institute for Molecular Genetics, Ihnestrasse 63-73, 14195, Berlin, Germany 5. Department of Bioinformatics, Max-Planck Institute for Molecular Genetics, Ihnestrasse 63-73, 14195, Berlin, Germany 8. Department of Medicine II, University of Freiburg Medical Center, Hugstetter Str. 55, 79106, Freiburg, Germany 2. Department of Pediatrics and Biocenter, University of Halle, Ernst-Grube-Str. 40, 06120, Halle (Saale), Germany 3. Department of Pathology, University of California, San Diego, School of Medicine, 9500 Gilman Drive, La Jolla, CA, 92093, USA 6. Department of Pharmacology I, University of Freiburg Medical Center, Albertstr. 25, 79106, Freiburg, Germany |
| Abstract: | Experimentation with PBX1 knockout mice has shown that PBX1 is necessary for early embryogenesis. Despite broad insight into PBX1 function, little is known about the underlying target gene regulation. Utilizing the Cre–loxP system, we targeted a functionally important part of the homeodomain of PBX1 through homozygous deletion of exon-6 and flanking intronic regions leading to exon 7 skipping in embryonic stem (ES) cells. We induced in vitro differentiation of wild-type and PBX1 mutant ES cells by aggregation and retinoic acid (RA) treatment and compared their profiles of gene expression at the ninth day post-reattachment to adhesive media. Our results indicate that PBX1 interactions with HOX proteins and DNA are dispensable for RA-induced ability of ES to express neural genes and point to a possible involvement of PBX1 in the regulation of imprinted genes. |
| Keywords: | |
| 本文献已被 SpringerLink 等数据库收录！ | |