PBX1 is dispensable for neural commitment of RA-treated murine ES cells

Jürgens, Anne S.; Kolanczyk, Mateusz; Moebest, Dietrich C. C.; Zemojtel, Tomasz; Lichtenauer, Urs; Duchniewicz, Marlena; Gantert, Melanie P.; Hecht, Jochen; Hattenhorst, Uwe; Burdach, Stefan; Dorn, Annette; Kamps, Mark P.; Beuschlein, Felix; Räpple, Daniel; Scheele, Jürgen S.

doi:10.1007/s11626-008-9162-5

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PBX1 is dispensable for neural commitment of RA-treated murine ES cells

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Kolanczyk, Mateusz
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Zemojtel, Tomasz
Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Hecht, Jochen
Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Citation

Jürgens, A. S., Kolanczyk, M., Moebest, D. C. C., Zemojtel, T., Lichtenauer, U., Duchniewicz, M., et al. (2009). PBX1 is dispensable for neural commitment of RA-treated murine ES cells. In Vitro Cellular & Developmental Biology - Animal, 45(5-6), 252-263. doi:10.1007/s11626-008-9162-5.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-7D9E-6

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.