Premium
Mammalian TAF II 30 is required for cell cycle progression and specific cellular differentiation programmes
Author(s) -
Metzger Daniel,
Scheer Elisabeth,
Soldatov Aleksey,
Tora Làszlò
Publication year - 1999
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/18.17.4823
Subject(s) - biology , null allele , retinoblastoma protein , cellular differentiation , null cell , microbiology and biotechnology , cre recombinase , cell cycle , gene expression , cyclin , gene , phenotype , genetics , transgene , genetically modified mouse
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.