TAF10 (TAF(II)30) is necessary for TFIID stability and early embryogenesis in mice.
Fiche publication
Date publication
juin 2003
Journal
Molecular and cellular biology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr METZGER Daniel, Dr TORA Laszlo
Tous les auteurs :
Mohan WS, Scheer E, Wendling O, Metzger D, Tora L
Lien Pubmed
Résumé
TAF10 (formerly TAF(II)30), is a component of TFIID and the TATA box-binding protein (TBP)-free TAF-containing complexes (TFTC/PCAF/STAGA). To investigate the physiological function of TAF10, we disrupted its gene in mice by using a Cre recombinase/LoxP strategy. Interestingly, no TAF10(-/-) animals were born from intercrosses of TAF10(+/-) mice, indicating that TAF10 is required for embryogenesis. TAF10(-/-) embryos developed to the blastocyst stage, implanted, but died shortly after ca. 5.5 days postcoitus. Surprisingly, trophoblast cells from TAF10(-/-) blastocysts were viable, whereas inner cell mass cells failed to survive, highlighting that TAF10 is not generally required for transcription in all cells. TAF10-deficient cells express normal levels of TBP and TAFs other than TAF10 but contain only partially formed TFIID, are endocycle arrested, and have undetectable levels of transcription. Thus, our results demonstrate that TAF10 is required for TFIID stability, cell cycle progression, and transcription in the early mouse embryo.
Mots clés
Alleles, Animals, Apoptosis, Blotting, Western, Bromodeoxyuridine, pharmacology, Cell Cycle, Cell Division, Cell Survival, Crosses, Genetic, DNA Nucleotidyltransferases, metabolism, Gene Expression Regulation, Developmental, Genotype, In Situ Hybridization, In Situ Nick-End Labeling, Mice, Mice, Transgenic, Microscopy, Fluorescence, Models, Genetic, Mutation, Phenotype, Phosphorylation, Precipitin Tests, Proteins, metabolism, RNA, metabolism, Recombinases, TATA-Binding Protein Associated Factors, genetics, Time Factors, Transcription Factor TFIID, chemistry, Trophoblasts, metabolism
Référence
Mol. Cell. Biol.. 2003 Jun;23(12):4307-18