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首页> 外文期刊>Molecular and Cellular Biology >Histone Acetyltransferase Activity of p300 Is Required for Transcriptional Repression by the Promyelocytic Leukemia Zinc Finger Protein
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Histone Acetyltransferase Activity of p300 Is Required for Transcriptional Repression by the Promyelocytic Leukemia Zinc Finger Protein

机译：p300的组蛋白乙酰转移酶活性是早幼粒细胞白血病锌指蛋白转录抑制所必需的。

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Histone acetyltransferase (HAT) activities of proteins such as p300, CBP, and P/CAF play important roles in activation of gene expression. We now show that the HAT activity of p300 can also be required for down-regulation of transcription by a DNA binding repressor protein. Promyelocytic leukemia zinc finger (PLZF), originally identified as a fusion with retinoic acid receptor alpha in rare cases of all-trans-retinoic acid-resistant acute promyelocytic leukemia, is a transcriptional repressor that recruits histone deacetylase-containing corepressor complexes to specific DNA binding sites. PLZF associates with p300 in vivo, and its ability to repress transcription is specifically dependent on HAT activity of p300 and acetylation of lysines in its C-terminal C2-H2 zinc finger motif. An acetylation site mutant of PLZF does not repress transcription and is functionally deficient in a colony suppression assay despite retaining its abilities to interact with corepressor/histone deacetylase complexes. This is due to the fact that acetylation of PLZF activates its ability to bind specific DNA sequences both in vitro and in vivo. Taken together, our results indicate that a histone deacetylase-dependent transcriptional repressor can be positively regulated through acetylation and point to an unexpected role of a coactivator protein in transcriptional repression.
机译：p300，CBP和P / CAF等蛋白质的组蛋白乙酰转移酶（HAT）活性在激活基因表达中起重要作用。现在我们表明，p300的HAT活性对于DNA结合阻遏蛋白的转录下调也可能是必需的。早幼粒细胞白血病锌指（PLZF）最初被确定为与视黄酸受体α融合，在罕见的全反式-维甲酸耐受性急性早幼粒细胞白血病中是一种转录阻遏物，其募集组蛋白脱乙酰基酶-含有针对特定DNA结合位点的corepressor复合物。 PLZF在体内与p300相关联，其抑制转录的能力特别取决于p300的HAT活性和其C末端C 2 -H 2 锌中赖氨酸的乙酰化手指图案。 PLZF的乙酰化位点突变体不抑制转录，并且在菌落抑制测定中功能上存在缺陷，尽管保留了其与共加压子/组蛋白脱乙酰基酶复合物相互作用的能力。这是由于以下事实：PLZF的乙酰化会在体外和体内激活其结合特定DNA序列的能力。两者合计，我们的结果表明，组蛋白脱乙酰基酶依赖的转录阻遏物可以通过乙酰化得到正调控，并指出了共激活蛋白在转录阻抑中的意想不到的作用。

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