Specific alterations of U1-C protein or U1 small nuclear RNA can eliminate the requirement of Prp28p, an essential DEAD box splicing factor
Specific alterations of U1-C protein or U1 small nuclear RNA can eliminate the requirement of Prp28p, an essential DEAD box splicing factor
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DOI：
10.1016/s1097-2765(01)00170-8
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发表时间：
2001-01-01
期刊：
影响因子：
16
通讯作者：
Chang, TH
中科院分区：
文献类型：
--
作者：
Chen, JYF;Stands, L;Chang, TH
虽然普遍存在的DExD/H盒蛋白家族的一些成员在体外具有RNA解旋酶活性，但它们在体内的作用几乎仍然未知。在这里，我们表明，否则必不可少的DEAD盒蛋白，Prp 28 p的功能，可以绕过突变，改变蛋白质U1-C或U1小核RNA。进一步的分析表明，U1-C蛋白中保守的L13残基特异性接触，以稳定前剪接体中的U1 snRNA/5'剪接位点双链体，Prp 28 p的功能是抵消U1-C蛋白的稳定作用，从而促进U1小核核糖核蛋白颗粒从5'剪接位点解离。因此，除了解旋RNA之外，DExD/H盒蛋白还可以通过拮抗特定的RNA稳定蛋白来影响RNA-RNA重排。
While some members of the ubiquitous DExD/H box family of proteins have RNA helicase activity in vitro, their roles in vivo remain virtually unknown. Here, we show that the function of an otherwise essential DEAD box protein, Prp28p, can be bypassed by mutations that alter either the protein U1-C or the U1 small nuclear RNA. Further analysis suggests that the conserved L13 residue in the U1-C protein makes specific contact to stabilize the U1 snRNA/5' splice site duplex in the prespliceosome, and that Prp28p functions to counteract the stabilizing effect of the U1-C protein, thereby promoting the dissociation of the U1 small nuclear ribonucleoprotein particle from the 5' splice site. Thus, in addition to unwinding RNA, the DExD/H box proteins may affect RNA-RNA rearrangements by antagonizing specific RNA-stabilizing proteins.