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p54nrb/NonO and PSF promote U snRNA nuclear export by accelerating its export complex assembly

机译:p54nrb / NonO和PSF通过加速其出口复合物组装促进U snRNA核出口

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The assembly of spliceosomal U snRNPs in metazoans requires nuclear export of U snRNA precursors. Four factors, nuclear cap-binding complex (CBC), phosphorylated adaptor for RNA export (PHAX), the export receptor CRM1 and RanGTP, gather at the m(7)G-cap-proximal region and form the U snRNA export complex. Here we show that the multifunctional RNA-binding proteins p54nrb/NonO and PSF are U snRNA export stimulatory factors. These proteins, likely as a heterodimer, accelerate the recruitment of PHAX, and subsequently CRM1 and Ran onto the RNA substrates in vitro, which mediates efficient U snRNA export in vivo. Our results reveal a new layer of regulation for U snRNA export and, hence, spliceosomal U snRNP biogenesis.
机译:后生动物中剪接体U snRNP的组装需要U snRNA前体的核输出。四个因素,核帽结合复合物(CBC),RNA出口磷酸化衔接子(PHAX),出口受体CRM1和RanGTP,聚集在m(7)G-cap-proximal区并形成U snRNA出口复合物。在这里我们显示多功能RNA结合蛋白p54nrb / NonO和PSF是U snRNA出口刺激因子。这些蛋白质可能是异二聚​​体,可加速PHAX的募集,并随后在体外将CRM1和Ran转移至RNA底物上,从而介导体内有效的U snRNA输出。我们的结果揭示了U snRNA出口以及因此剪接的U snRNP生物发生的新一层调控。

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