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首页> 外文期刊>Genes & Genetic Systems >Interplay between chromatin modulators and histone acetylation regulates the formation of accessible chromatin in the upstream regulatory region of fission yeast fbp1
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Interplay between chromatin modulators and histone acetylation regulates the formation of accessible chromatin in the upstream regulatory region of fission yeast fbp1

机译:染色质调节剂和组蛋白乙酰化之间的相互作用调节裂变酵母fbp1上游调控区中可及的染色质的形成。

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摘要

Numerous noncoding RNA transcripts are detected in eukaryotic cells. Noncoding RNAs transcribed across gene promoters are involved in the regulation of mRNA transcription via chromatin modulation. This function of noncoding RNA transcription was first demonstrated for the fission yeast fbp1 gene, where a cascade of noncoding RNA transcription events induces chromatin remodeling to facilitate transcription factor binding. We recently demonstrated that the noncoding RNAs from the fbp1 upstream region facilitate binding of the transcription activator Atf1 and thereby promote histone acetylation. Histone acetylation by histone acetyl transferases (HATs) and ATP-dependent chromatin remodelers (ADCRs) are implicated in chromatin remodeling, but the interplay between HATs and ADCRs in this process has not been fully elucidated. Here, we examine the roles played by two distinct ADCRs, Snf22 and Hrp3, and by the HAT Gcn5 in the transcriptional activation of fbp1. Snf22 and Hrp3 redundantly promote disassembly of chromatin in the fbp1 upstream region. Gcn5 critically contributes to nucleosome eviction in the absence of either Snf22 or Hrp3, presumably by recruiting Hrp3 in snf22a?? cells and Snf22 in hrp3a?? cells. Conversely, Gcn5-dependent histone H3 acetylation is impaired in snf22a??/hrp3a?? cells, suggesting that both redundant ADCRs induce recruitment of Gcn5 to the chromatin array in the fbp1 upstream region. These results reveal a previously unappreciated interplay between ADCRs and histone acetylation in which histone acetylation facilitates recruitment of ADCRs, while ADCRs are required for histone acetylation.
机译:在真核细胞中检测到许多非编码RNA转录物。跨基因启动子转录的非编码RNA通过染色质调节参与mRNA转录的调控。裂变酵母fbp1基因首次证明了非编码RNA转录的这种功能,其中级联的非编码RNA转录事件诱导了染色质重塑,从而促进了转录因子的结合。我们最近证明了来自fbp1上游区域的非编码RNA促进了转录激活因子Atf1的结合,从而促进了组蛋白的乙酰化。组蛋白乙酰基转移酶(HATs)和ATP依赖的染色质重塑剂(ADCRs)引起的组蛋白乙酰化与染色质重塑有关,但是在此过程中HATs和ADCR之间的相互作用尚未得到充分阐明。在这里,我们检查了两个不同的ADCR,Snf22和Hrp3,以及HAT Gcn5在fbp1的转录激活中所起的作用。 Snf22和Hrp3冗余地促进fbp1上游区域中的染色质分解。在不存在Snf22或Hrp3的情况下,Gcn5关键地促进了核小体的逐出,大概是通过在snf22a中募集Hrp3来实现的。 hrp3a细胞和Snf22?细胞。相反,在snf22aβ/hrp3aβ中,Gcn5依赖性组蛋白H3乙酰化受到损害。细胞,这表明两个冗余ADCR诱导Gcn5募集到fbp1上游区域的染色质阵列。这些结果揭示了ADCR和组蛋白乙酰化之间以前未被认识的相互作用,其中组蛋白乙酰化促进ADCR的募集,而组蛋白乙酰化则需要ADCR。

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