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Regulation of Alternative Polyadenylation by U1 snRNPs and SRp20

机译：U1 snRNPs和SRp20对替代性聚腺苷酸的调控

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Although considerable information is currently available about the factors involved in constitutive vertebrate polyadenylation, the factors and mechanisms involved in facilitating communication between polyadenylation and splicing are largely unknown. Even less is known about the regulation of polyadenylation in genes in which 3′-terminal exons are alternatively recognized. Here we demonstrate that an SR protein, SRp20, affects recognition of an alternative 3′-terminal exon via an effect on the efficiency of binding of a polyadenylation factor to an alternative polyadenylation site. The gene under study codes for the peptides calcitonin and calcitonin gene-related peptide. Its pre-mRNA is alternatively processed by the tissue-specific inclusion or exclusion of an embedded 3′-terminal exon, exon 4, via factors binding to an intronic enhancer element that contains both 3′ and 5′ splice site consensus sequence elements. In cell types that preferentially exclude exon 4, addition of wild-type SRp20 enhances exon 4 inclusion via recognition of the intronic enhancer. In contrast, in cell types that preferentially include exon 4, addition of a mutant form of SRp20 containing the RNA-binding domain but missing the SR domain inhibits exon 4 inclusion. Inhibition is likely at the level of polyadenylation, because the mutant SRp20 inhibits binding of CstF to the exon 4 poly(A) site. This is the first demonstration that an SR protein can influence alternative polyadenylation and suggests that this family of proteins may play a role in recognition of 3′-terminal exons and perhaps in the communication between polyadenylation and splicing.
机译：尽管目前可获得有关组成型脊椎动物聚腺苷酸化的因素的大量信息，但在很大程度上尚不清楚促进聚腺苷酸化和剪接之间交流的因素和机制。关于在其中交替识别3'-末端外显子的基因中对聚腺苷酸化的调控了解甚少。在这里，我们证明了SR蛋白SRp20通过影响多腺苷酸化因子与另一种多腺苷酸化位点结合的效率，影响对另一种3'-末端外显子的识别。研究中的基因编码降钙素和降钙素基因相关肽。或者，通过与包含3'和5'剪接位点共有序列元件的内含子增强子元件结合的因子，通过嵌入的3'-末端外显子，外显子4的组织特异性包含或排除，来处理其前mRNA。在优先排除外显子4的细胞类型中，添加野生型SRp20可通过识别内含子增强子来增强外显子4的包容性。相反，在优先包括外显子4的细胞类型中，添加包含RNA结合结构域但缺少SR结构域的SRp20突变形式会抑制外显子4的包涵。抑制可能是在聚腺苷酸水平，因为突变体SRp20抑制CstF与外显子4 poly（A）位点的结合。这是第一个证明SR蛋白可以影响替代性聚腺苷酸化的证据，并表明该蛋白家族可能在识别3'末端外显子以及可能在聚腺苷酸化和剪接之间的交流中发挥作用。

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