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首页> 外文期刊>Molecular and Cellular Biology >Retroviral Splicing Suppressor Sequesters a 3′ Splice Site in a 50S Aberrant Splicing Complex
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Retroviral Splicing Suppressor Sequesters a 3′ Splice Site in a 50S Aberrant Splicing Complex

机译：逆转录病毒剪接抑制剂在50s异常拼接复合物中螯合3'拼接部位

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摘要

Retroviral replication requires both spliced and unspliced mRNAs. Splicing suppression of avian retroviral RNA depends in part upon a cis-acting element within the gag gene called the negative regulator of splicing (NRS). The NRS, linked to a downstream intron and exon (NRS-Ad3′), was not capable of splicing in vitro. However, a double-point mutation in the NRS pseudo-5′ splice site sequence converted it into a functional 5′ splice site. The wild-type (WT) NRS-Ad3′ transcript assembled an ～50S spliceosome-like complex in vitro; its sedimentation rate was similar to that of a functional spliceosome formed on the mutant NRS-Ad3′ RNA. The five major spliceosomal snRNPs were observed in both complexes by affinity selection. In addition, U11 snRNP was present only in the WT NRS-Ad3′ complex. Addition of heparin to these complexes destabilized the WT NRS-Ad3′ complex; it was incapable of forming a B complex on a native gel. Furthermore, the U5 snRNP protein, hPrp8, did not cross-link to the NRS pseudo-5′ splice site, suggesting that the tri-snRNP complex was not properly associated with it. We propose that this aberrant, stalled spliceosome, containing U1, U2, and U11 snRNPs and a loosely associated tri-snRNP, sequesters the 3′ splice site and prevents its interaction with the authentic 5′ splice site upstream of the NRS.
机译：逆转录病毒复制需要拼接和未过敏的MRNA。抗逆转录病毒RNA的剪接抑制在 Gag 基因内部分依赖于称为剪接负调节剂（NRS）的 Gag 基因内的 CIS -Acting元素。与下游内含子和外显子（NRS-AD3'）相关的NRS不能在体外拼接。然而，NRS伪5'剪接部位序列中的双点突变将其转换为功能5'拼接部位。野生型（WT）NRS-AD3'转录物在体外组装了〜50s抗体组合体的复合物;其沉降率类似于形成在突变NRS-AD3'RNA上形成的功能性抗磷酸体的沉降速率。通过亲和选择在两种复合物中观察到五个主要的抗乳糖体SnRNP。此外，U11 SNRNP仅存在于WT NRS-AD3'复合物中。向这些复合物中添加肝素破坏了WT NRS-AD3'复合物;它不能在天然凝胶上形成B络合物。此外，U5 SNRNP蛋白HPRP8与NRS伪5'接头位点没有交联，表明TRI-SNRNP复合物没有与其正确相关。我们提出这种异常，含有U1，U2和U11 SNRNP和松散相关的三-SNRNP的这种异常，停滞的抗乳头组，螯合3'剪接部位并防止其与NR上游的真实5'接头位点的相互作用。

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