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首页> 外文期刊>Molecular and Cellular Biology >Regulation of Nucleolar Chromatin by B23/Nucleophosmin Jointly Depends upon Its RNA Binding Activity and Transcription Factor UBF
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Regulation of Nucleolar Chromatin by B23/Nucleophosmin Jointly Depends upon Its RNA Binding Activity and Transcription Factor UBF

机译：B23 /核糖蛋白对核仁染色质的调节共同取决于其RNA结合活性和转录因子UBF。

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摘要

Histone chaperones regulate the density of incorporated histone proteins around DNA transcription sites and therefore constitute an important site-specific regulatory mechanism for the control of gene expression. At present, the targeting mechanism conferring this site specificity is unknown. We previously reported that the histone chaperone B23ucleophosmin associates with rRNA chromatin (r-chromatin) to stimulate rRNA transcription. Here, we report on the mechanism for site-specific targeting of B23 to the r-chromatin. We observed that, during mitosis, B23 was released from chromatin upon inactivation of its RNA binding activity by cdc2 kinase-mediated phosphorylation. The phosphorylation status of B23 was also shown to strongly affect its chromatin binding activity. We further found that r-chromatin binding of B23 was a necessary condition for B23 histone chaperone activity in vivo. In addition, we found that depletion of upstream binding factor (UBF; an rRNA transcription factor) decreased the chromatin binding affinity of B23, which in turn led to an increase in histone density at the r-chromatin. These two major strands of evidence suggest a novel cell cycle-dependent mechanism for the site-specific regulation of histone density via joint RNA- and transcription factor-mediated recruitment of histone chaperones to specific chromosome loci.
机译：组蛋白伴侣调节DNA转录位点周围掺入的组蛋白的密度，因此构成控制基因表达的重要位点特异性调节机制。目前，赋予该位点特异性的靶向机制尚不清楚。我们以前曾报道过，组蛋白伴侣B23 /核蛋白与rRNA染色质（r-chromatin）缔合，以刺激rRNA转录。在这里，我们报告了针对R23染色质的B23的位点特异性靶向机制。我们观察到，在有丝分裂过程中，由于cdc2激酶介导的磷酸化使RNA结合活性失活，染色质释放了B23。还显示出B23的磷酸化状态强烈影响其染色质结合活性。我们进一步发现，B23的r-染色质结合是B23体内组蛋白伴侣活性 的必要条件。此外，我们发现上游结合因子（UBF; rRNA转录因子）的消耗降低了B23的染色质结合亲和力，进而导致r-染色质上组蛋白密度增加。这两个主要证据表明，通过联合RNA和转录因子介导的组蛋白伴侣到特定染色体位点的募集，新的细胞周期依赖性机制可用于组蛋白密度的位点特异性调节。

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