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在体内GAL1转录激活过程中,GAL4会破坏一个抑制性核小体。

GAL4 disrupts a repressing nucleosome during activation of GAL1 transcription in vivo.

作者信息

Axelrod J D, Reagan M S, Majors J

机构信息

Department of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, Missouri 63110.

出版信息

Genes Dev. 1993 May;7(5):857-69. doi: 10.1101/gad.7.5.857.

Abstract

Photofootprinting in vivo of GAL1 reveals an activation-dependent pattern between the UASG and the TATA box, in a sequence not required for transcriptional activation by GAL4. The pattern results from a nucleosome whose position depends on sequences within the UASG. In the wild-type gene, activation by GAL4 and derivatives disrupts this nucleosome. This activity is independent of interactions with DNA-bound core transcription factors and is proportional to the strength of the activator. Presence of the nucleosome correlates with low basal transcription levels under various conditions, suggesting a role in limiting basal expression. We propose a role for the GAL4 activation domain in displacing a nucleosome and suggest that this is part of the mechanism by which GAL4 activates transcription in vivo.

摘要

GAL1在体内的光足迹分析揭示了UASG和TATA框之间一种依赖于激活的模式,该模式存在于GAL4转录激活所不需要的序列中。这种模式源于一个核小体,其位置取决于UASG内的序列。在野生型基因中,GAL4及其衍生物的激活会破坏这个核小体。这种活性独立于与DNA结合的核心转录因子的相互作用,并且与激活剂的强度成正比。核小体的存在与各种条件下的低基础转录水平相关,表明其在限制基础表达中起作用。我们提出GAL4激活域在取代核小体中发挥作用,并认为这是GAL4在体内激活转录机制的一部分。

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