Mammalian polycomb-mediated repression of Hox genes requires the essential spliceosomal protein Sf3b1

Mammalian polycomb-mediated repression of Hox genes requires the essential spliceosomal protein Sf3b1
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DOI:
10.1101/gad.1284605
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发表时间:
2005-03-01
影响因子:
10.5
通讯作者:
Koseki, H
Koseki, H
中科院分区:
生物学1区
文献类型:
--
作者:
Isono, K;Mizutani-Koseki, Y;Koseki, H

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Polycomb group (PcG)蛋白通过形成多聚体蛋白复合物来稳定抑制同源性(Hox)基因。我们展示了(1)U2小核核糖核蛋白颗粒(U2 snRNP)组分之间的物理相互作用,包括Sf3bl和PcG蛋白Zfp144和Rnf2;(2) sf3b1杂合小鼠在异位Hox表达的同时表现出骨骼转化。这些改变被Zfpl44突变增强,而被M11突变(一个三胸群基因)抑制。重要的是,在sf3b1杂合胚胎中,PcG复合物中Sf3bI的水平降低。这些发现表明Sf3b1-PcG蛋白相互作用对于真正的pcg介导的Hox基因抑制至关重要。
Polycomb group (PcG) proteins are responsible for the stable repression of homeotic (Hox) genes by forming multimeric protein complexes. We show (1) physical interaction between components of the U2 small nuclear ribonucleoprotein particle (U2 snRNP), including Sf3bl and PcG proteins Zfp144 and Rnf2; and (2) that Sf3b1-heterozygous mice exhibit skeletal transformations concomitant with ectopic Hox expressions. These alterations are enhanced by Zfpl44 mutation but repressed by M11 mutation (a trithorax-group gene). Importantly, the levels of Sf3bI in PcG complexes were decreased in Sf3b1-heterozygous embryos. These findings suggest that Sf3b1-PcG protein interaction is essential for true PcG-mediated repression of Hox genes.