| First Author | Metzger D | Year | 1999 |
| Journal | EMBO J | Volume | 18 |
| Issue | 17 | Pages | 4823-34 |
| PubMed ID | 10469660 | Mgi Jnum | J:57447 |
| Mgi Id | MGI:1344821 | Doi | 10.1093/emboj/18.17.4823 |
| Citation | Metzger D, et al. (1999) Mammalian TAF(II)30 is required for cell cycle progression and specific cellular differentiation programmes. EMBO J 18(17):4823-34 |
| abstractText | 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. |
