Mammalian TAF(II)30 is required for cell cycle progression and specific cellular differentiation programmes.
Fiche publication
Date publication
septembre 1999
Journal
The EMBO journal
Auteurs
Membres identifiés du Cancéropôle Est :
Dr METZGER Daniel, Dr TORA Laszlo
Tous les auteurs :
Metzger D, Scheer E, Soldatov A, Tora L
Lien Pubmed
Résumé
The two alleles of the 30 kDa TATA-binding protein associated factor (TAF(II)30) gene, have been targeted by homologous recombination in murine F9 embryonal carcinoma cells and subsequently disrupted using a Cre recombinase-loxP strategy. The TAF(II)30-null cells are not viable, but are rescued by the expression of human TAF(II)30. Cells lacking TAF(II)30 are blocked in G(1)/G(0) phase of the cell cycle and undergo apoptosis. In agreement with the G(1) arrest phenotype, the expression of cyclin E is impaired and the retinoblastoma protein is hypophosphorylated in the TAF(II)30-null cells. Interestingly, retinoic acid (RA) treatment prevented TAF(II)30-null cell death and induced primitive endodermal differentiation. In contrast, the RA- and cAMP-induced parietal endodermal differentiation was impaired in the TAF(II)30-null cells. Thus, TAF(II)30 is not indispensable for class II gene transcription in general, but seems to be required for the expression of a subset of genes.
Mots clés
Animals, Antineoplastic Agents, pharmacology, Apoptosis, Carcinoma, Embryonal, genetics, Cell Cycle, physiology, Cell Differentiation, physiology, Cell Division, physiology, DNA-Binding Proteins, physiology, Gene Expression Regulation, Developmental, Gene Expression Regulation, Neoplastic, Integrases, metabolism, Mice, Mice, Knockout, Models, Genetic, Mutagenesis, Insertional, Stem Cells, cytology, TATA-Binding Protein Associated Factors, Time Factors, Transcription Factor TFIID, Transcription Factors, physiology, Tretinoin, pharmacology, Tumor Cells, Cultured, Viral Proteins
Référence
EMBO J.. 1999 Sep 1;18(17):4823-34