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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Upstream binding factor association induces large-scale chromatin decondensation
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Upstream binding factor association induces large-scale chromatin decondensation

机译：上游结合因子缔合导致大规模的染色质缩聚

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摘要

The function of upstream binding factor (UBF), an essential component of the RNA polymerase (pol) I preinitiation complex, is unclear. Recently, UBF was found distributed throughout ribosomal gene repeats rather than being restricted to promoter regions. This observation has led to the speculation that one role of UBF binding may be to induce chromatin remodeling. To directly evaluate the impact of UBF on chromatin structure, we used an in vivo assay in which UBF is targeted via a lac repressor fusion protein to a heterochromatic, amplified chromosome region containing lac operator repeats. We show that the association of UBF with this locus induces large-scale chromatin decondensation. This process does not appear to involve common remodeling complexes, including SWI/SNF and histone acetyltransferases, and is independent of histone H3 lysine 9 acetylation. However, UBF recruits the pol I-specific, TATA box-binding protein containing complex SL1 and pol I subunits. Our results suggest a working hypothesis in which the dynamic association of UBF with ribosomal DNA clusters recruits the pol I transcription machinery and maintains these loci in a transcriptionally competent configuration. These studies also provide an in vivo model simulating ribosomal DNA transactivation outside the nucleolus, allowing temporal and spatial analyses of chromatin remodeling and assembly of the pol I transcription machinery.
机译：上游结合因子（UBF）的功能尚不清楚，上游结合因子（UBF）是RNA聚合酶（pol）I预启动复合物的重要组成部分。最近，发现UBF分布在整个核糖体基因重复序列中，而不是局限于启动子区域。这一发现导致人们猜测，UBF结合的一种作用可能是诱导染色质重塑。为了直接评估UBF对染色质结构的影响，我们使用了一种体内测定方法，其中UBF通过lac阻遏物融合蛋白靶向包含lac操纵子重复序列的异色扩增染色体区域。我们表明，UBF与该基因座的关联会导致大规模染色质的缩聚。此过程似乎不涉及常见的重塑复合物，包括SWI / SNF和组蛋白乙酰转移酶，并且独立于组蛋白H3赖氨酸9乙酰化。但是，UBF募集了含有复杂SL1和pol I亚基的pol I特异性TATA盒结合蛋白。我们的研究结果提出了一个可行的假设，其中UBF与核糖体DNA簇的动态关联会募集pol I转录机制，并将这些基因座保持在转录能力上。这些研究还提供了在核仁外部模拟核糖体DNA反式激活的体内模型，从而可以对染色质重塑和pol I转录机制的组装进行时空分析。

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