REGULATION OF ALTERNATIVE SPLICING IN-VIVO BY OVEREXPRESSION OF ANTAGONISTIC SPLICING FACTORS
REGULATION OF ALTERNATIVE SPLICING IN-VIVO BY OVEREXPRESSION OF ANTAGONISTIC SPLICING FACTORS
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DOI：
10.1126/science.8085156
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发表时间：
1994-09-16
期刊：
影响因子：
56.9
通讯作者：
KRAINER, AR
中科院分区：
文献类型：
--
作者：
CACERES, JF;STAMM, S;KRAINER, AR
SF2/ASF和不均一核糖核蛋白（hnRNP）A1的相反作用在体外影响可变剪接。在海拉细胞中瞬时过度表达SF2/ASF或hnRNP A1互补DNA，并测量其对几个共转染报告基因可变剪接的影响。SF2/ASF表达增加激活近端5'剪接位点，促进一个神经元特异性外显子的包含，并防止异常外显子跳跃。hnRNP A1表达增加激活远端5'剪接位点。因此，细胞内拮抗剪接因子水平的变化影响体内可变剪接的不同模式，并且可能是基因表达的组织特异性或发育调控的一种自然机制。
The opposing effects of SF2/ASF and heterogeneous nuclear ribonucleoprotein (hnRNP) A1 influence alternative splicing in vitro. SF2/ASF or hnRNP A1 complementary DNAs were transiently overexpressed in HeLa cells, and the effect on alternative splicing of several cotransfected reporter genes was measured. Increased expression of SF2/ASF activated proximal 5' splice sites, promoted inclusion of a neuron-specific exon, and prevented abnormal exon skipping. Increased expression of hnRNP A1 activated distal 5' splice sites. Therefore, variations in the intracellular levels of antagonistic splicing factors influence different modes of alternative splicing in vivo and may be a natural mechanism for tissue-specific or developmental regulation of gene expression.