May M, Mengus G, Lavigne A C, Chambon P, Davidson I
Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, France.
EMBO J. 1996 Jun 17;15(12):3093-104.
Transcriptional activation in vitro involves direct interactions of transactivators with the TATA binding protein (TBP) and the TBP-associated factors (TAF(II)s) which constitute the TFIID complex. However, the role of TAF(II)s in transcriptional regulation in mammalian cells has not been addressed. We show that activation function 2 of the retinoid X receptors (RXR AF-2) does not activate transcription from a minimal promoter in Cos cells. However, coexpression of human (h) TAF(II)28 promotes a strong ligand-dependent activity of the RXR AF-2 on a minimal promoter and potentiates the ability of the RXRalpha AF-2 to activate transcription from a complex promoter. The expression of hTAF(II)28 also potentiated transactivation by several nuclear receptors, notably the oestrogen and vitamin D3 receptors (ER and VDR), whereas other classes of activator were not affected. The effect of hTAFII(28) on RXR AF-2 activities did not appear to require direct RXR-TAFII(28) interactions, but correlated with the ability of hTAFII(28) to interact with TBP. In contrast to Cos cells, the RXR AF-2s had differential abilities to activate transcription from a minimal promoter in HeLa cells, and a lesser increase in their activity was observed upon hTAFII28 coexpression. Moreover, coexpression of hTAFII(28) did not increase but rather repressed activation by the ER and VDR AF-2s in HeLa cells. In agreement with these data, showing that TAF(II)28 is limiting in the AF-2 activation pathway in Cos cells, TAF(II)28 is selectively depleted in Cos cell TFIID.
体外转录激活涉及反式激活因子与TATA结合蛋白（TBP）以及构成TFIID复合物的TBP相关因子（TAF（II）s）的直接相互作用。然而，TAF（II）s在哺乳动物细胞转录调控中的作用尚未得到研究。我们发现，维甲酸X受体的激活功能2（RXR AF-2）不能激活Cos细胞中最小启动子的转录。然而，共表达人（h）TAF（II）28可促进RXR AF-2在最小启动子上产生强烈的配体依赖性活性，并增强RXRα AF-2从复合启动子激活转录的能力。hTAF（II）28的表达还增强了几种核受体的反式激活作用，特别是雌激素和维生素D3受体（ER和VDR），而其他类型的激活剂则不受影响。hTAFII（28）对RXR AF-2活性的影响似乎不需要RXR与TAFII（28）直接相互作用，但与hTAFII（28）与TBP相互作用的能力相关。与Cos细胞不同，RXR AF-2在HeLa细胞中激活最小启动子转录的能力存在差异，共表达hTAFII28后其活性增加较少。此外，在HeLa细胞中共表达hTAFII（28）并没有增强反而抑制了ER和VDR AF-2的激活作用。与这些数据一致，表明TAF（II）28在Cos细胞的AF-2激活途径中是有限的，TAF（II）28在Cos细胞TFIID中被选择性消耗。
