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Subnuclear segregation of genes and core promoter factors in myogenesis.

机译:基因和核心启动子因子在核发生中的亚核分离。

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摘要

Recent findings implicate alternate core promoter recognition complexes in regulating cellular differentiation. Here we report a spatial segregation of the alternative core factor TAF3, but not canonical TFIID subunits, away from the nuclear periphery, where the key myogenic gene MyoD is preferentially localized in myoblasts. This segregation is correlated with the differential occupancy of TAF3 versus TFIID at the MyoD promoter. Loss of this segregation by modulating either the intranuclear location of the MyoD gene or TAF3 protein leads to altered TAF3 occupancy at the MyoD promoter. Intriguingly, in differentiated myotubes, the MyoD gene is repositioned to the nuclear interior, where TAF3 resides. The specific high-affinity recognition of H3K4Me3 by the TAF3 PHD (plant homeodomain) finger appears to be required for the sequestration of TAF3 to the nuclear interior. We suggest that intranuclear sequestration of core transcription components and their target genes provides an additional mechanism for promoter selectivity during differentiation.
机译:最近的发现暗示替代核心启动子识别复合物调节细胞分化。在这里,我们报告了替代核心因子TAF3的空间分离,但不是规范的TFIID亚基,远离核外围,其中关键的成肌基因MyoD优先位于成肌细胞中。这种分离与在MyoD启动子上TAF3与TFIID的差异占有率相关。通过调节MyoD基因或TAF3蛋白的核内位置而失去这种分离,会导致MyoD启动子上的TAF3占有率发生变化。有趣的是,在分化的肌管中,MyoD基因被重新定位到TAF3所在的核内部。 TAF3 PHD(植物同源域)手指对H3K4Me3的特定高亲和力识别似乎是将TAF3螯合到核内部所需的。我们建议核心转录成分及其靶基因的核内隔离为分化过程中的启动子选择性提供了额外的机制。

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