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RNA POLYMERASE II AS A LINK BETWEEN ALTERNATIVE SPLICING AND CHROMATIN STRUCTURE

机译:RNA聚合酶II作为交替剪接和染色质结构之间的联系

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摘要

Alternative splicing is a crucial mechanism to generate complexity of the proteome, yet its regulation is an open puzzle. Recent evidence indicates that signature of histone modifications and nucleosome positioning may cause splice site switching, suggesting RNA polymerase IKRNAP II) may mediate the link. Here we present analyses of RNAP II islands and nucleosome enrichment level around skipped exon(SE) 3' splicing sites and constitutive exon(CE) 3' splicing sites(3' ss). We have found histone modification plays more important role in slowing down RNAP II around SE 3' ss in contrast to CE 3' ss. Then we examined whether histone marking around these sites were special, finding that H3K4me3, H4K20mel and H3K27ac marks were different around SE and CE 3' ss in CD4+ T celL.
机译:选择性剪接是产生蛋白质组复杂性的关键机制,但其调控是一个难题。最近的证据表明,组蛋白修饰和核小体定位的特征可能会导致剪接位点转换,这表明RNA聚合酶(IKRNAP II)可能介导了这一联系。在这里,我们介绍了RNAP II岛和跳过的外显子(SE)3'剪接位点和本构外显子(CE)3'剪接位点(3'ss)附近的核小体富集水平的分析。我们发现,与CE 3's相比,组蛋白修饰在减缓SE 3's附近的RNAP II方面起着更重要的作用。然后,我们检查了这些位点周围的组蛋白标记是否特殊,发现CD4 + T celL中SE和CE 3's周围的H3K4me3,H4K20mel和H3K27ac标记不同。

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