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Mechanism of Polymerase II Transcription Repression by the Histone Variant macroH2A

机译：组蛋白变体macroH2A抑制聚合酶II转录的机制

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摘要

macroH2A (mH2A) is an unusual histone variant consisting of a histone H2A-like domain fused to a large nonhistone region. In this work, we show that histone mH2A represses p300- and Gal4-VP16-dependent polymerase II transcription, and we have dissected the mechanism by which this repression is realized. The repressive effect of mH2A is observed at the level of initiation but not at elongation of transcription, and mH2A interferes with p300-dependent histone acetylation. The nonhistone region of mH2A is responsible for both the repression of initiation of transcription and the inhibition of histone acetylation. In addition, the presence of this domain of mH2A within the nucleosome is able to block nucleosome remodeling and sliding of the histone octamer to neighboring DNA segments by the remodelers SWI/SNF and ACF. These data unambiguously identify mH2A as a strong transcriptional repressor and show that the repressive effect of mH2A is realized on at least two different transcription activation chromatin-dependent pathways: histone acetylation and nucleosome remodeling.
机译：macroH2A（mH2A）是一种不常见的组蛋白变体，由与大的非组蛋白区域融合的组蛋白H2A样结构域组成。在这项工作中，我们表明组蛋白mH2A抑制p300和Gal4-VP16依赖的聚合酶II转录，并且我们已经剖析了实现这种抑制的机制。在起始水平观察到mH2A的抑制作用，但在转录延伸时未观察到，并且mH2A干扰p300依赖的组蛋白乙酰化。 mH2A的非组蛋白区域负责转录起始的抑制和组蛋白乙酰化的抑制。另外，核小体中mH2A结构域的存在能够阻止核小体重塑，并通过重塑剂SWI / SNF和ACF阻止组蛋白八聚体滑向邻近的DNA片段。这些数据明确地将mH2A鉴定为强转录阻遏物，并表明mH2A的抑制作用是通过至少两种不同的转录激活染色质依赖性途径实现的：组蛋白乙酰化和核小体重塑。

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