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Mammalian TAFII30 is required for cell cycle progression and specific cellular differentiation programmes

The two alleles of the 30 kDa TATA‐binding protein associated factor (TAFII30) gene, have been targeted by homologous recombination in murine F9 embryonal carcinoma cells and subsequently disrupted using a Cre recombinase–loxP strategy. The TAFII30‐null cells are not viable, but are rescued by the expression of human TAFII30. Cells lacking TAFII30 are blocked in G1/G0 phase of the cell cycle and undergo apoptosis. In agreement with the G1 arrest phenotype, the expression of cyclin E is impaired and the retinoblastoma protein is hypophosphorylated in the TAFII30‐null cells. Interestingly, retinoic acid (RA) treatment prevented TAFII30‐null cell death and induced primitive endodermal differentiation. In contrast, the RA‐ and cAMP‐induced parietal endodermal differentiation was impaired in the TAFII30‐null cells. Thus, TAFII30 is not indispensable for class II gene transcription in general, but seems to be required for the expression of a subset of genes.