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首页> 外文期刊>Molecular and Cellular Biology >p300 Requires Its Histone Acetyltransferase Activity and SRC-1 Interaction Domain To Facilitate Thyroid Hormone Receptor Activation in Chromatin
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p300 Requires Its Histone Acetyltransferase Activity and SRC-1 Interaction Domain To Facilitate Thyroid Hormone Receptor Activation in Chromatin

机译：p300需要其组蛋白乙酰转移酶活性和SRC-1相互作用域，以促进染色质中的甲状腺激素受体活化。

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We have characterized the mechanism by which coactivator p300 facilitates transcriptional activation mediated by the heterodimer of thyroid hormone (T3) receptor and 9-cis retinoid acid receptor (TR-RXR) in the context of chromatin. We demonstrate that, while p300 can enhance the transcriptional activation mediated by both liganded TR-RXR and GAL4-VP16, its histone acetyltransferase activity (HAT) is required for its ability to facilitate liganded TR-RXR- but not GAL4-VP16-mediated transcriptional activation. To understand how p300 is recruited by liganded TR-RXR, we have analyzed the interactions between TR-RXR and p300 as well as SRC-1 family coactivators. We show that, in contrast to a strong hormone-dependent interaction between TR-RXR and SRC-1 family coactivators, p300 displays minimal, if any, T3-dependent interaction with TR-RXR. However, p300 can be recruited by liganded TR-RXR through its interaction with SRC-1 family coactivators. Consistent with the protein-protein interaction profile described above, we demonstrate that the SRC-1 interaction domain of p300 is important for its ability to facilitate transcriptional activation mediated by TR-RXR, whereas its nuclear receptor interaction domain is dispensable. Collectively, these results reveal the functional significance of the HAT activity of p300 and define an indirect mode for the action of p300 in TR-RXR activation.
机译：我们已经表征了在染色质的背景下，共激活因子p300促进由甲状腺激素（T3）受体和9- 顺式类视黄酸受体（TR-RXR）的异二聚体介导的转录激活的机制。我们证明，虽然p300可以增强由配体TR-RXR和GAL4-VP16介导的转录激活，但其组蛋白乙酰转移酶活性（HAT）是其促进配体TR-RXR-而不是GAL4-VP16介导的转录的能力所必需的激活。为了了解配体TR-RXR如何募集p300，我们分析了TR-RXR与p300以及SRC-1家族共激活因子之间的相互作用。我们显示，与TR-RXR和SRC-1家族共激活剂之间强烈的激素依赖性相互作用相反，p300与TR-RXR的T3依赖性相互作用最小（如果有的话）。但是，p300可以通过配体TR-RXR与SRC-1家族共激活因子的相互作用而募集。与上述蛋白质-蛋白质相互作用概况一致，我们证明p300的SRC-1相互作用域对于促进由TR-RXR介导的转录激活的能力很重要，而其核受体相互作用域则是可有可无的。这些结果共同揭示了p300的HAT活性的功能意义，并为p300在TR-RXR激活中的作用定义了间接模式。

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