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首页> 外文期刊>Molecular and Cellular Biology >Effects of histone acetylation on chromatin topology in vivo.
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Effects of histone acetylation on chromatin topology in vivo.

机译：组蛋白乙酰化对体内染色质拓扑的影响。

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Recently a model for eukaryotic transcriptional activation has been proposed in which histone hyperacetylation causes release of nucleosomal supercoils, and this unconstrained tension in turn stimulates transcription (V. G. Norton, B. S. Imai, P. Yau, and E. M. Bradbury, Cell 57:449-457, 1989; V. G. Norton, K. W. Marvin, P. Yau, and E. M. Bradbury, J. Biol. Chem. 265:19848-19852, 1990). These studies analyzed the effect of histone hyperacetylation on the change in topological linking number which occurs during nucleosome assembly in vitro. We have tested this model by determining the effect of histone hyperacetylation on the linking number change which occurs during assembly in vivo. We find that butyrate treatment of cells infected with simian virus 40 results in hyperacetylation of the histones of the extracted viral minichromosome as expected. However, the change in constrained supercoils of the minichromosome DNA is minimal, a result which is inconsistent with the proposed model. These results indicate that the proposed mechanism of transcriptional activation is unlikely to take place in the cell.
机译：最近，有人提出了一种用于真核转录激活的模型，其中组蛋白超乙酰化导致核小体超螺旋的释放，这种不受约束的张力反过来又刺激了转录（VG Norton，BS Imai，P。Yau和EM Bradbury，Cell 57：449-457， 1989; VG Norton，KW Marvin，P.Yau，和EM Bradbury，J.Biol.Chem.265：19848-19852，1990）。这些研究分析了组蛋白超乙酰化对体外核小体组装过程中发生的拓扑连接数变化的影响。我们通过确定组蛋白超乙酰化对体内组装过程中发生的连接数变化的影响来测试该模型。我们发现丁酸处理的猿猴病毒40感染的细胞导致提取的病毒微型染色体组蛋白的超乙酰化，如预期的那样。但是，微型染色体DNA的受约束超螺旋变化很小，结果与所提出的模型不一致。这些结果表明拟议的转录激活机制不太可能在细胞中发生。

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