A NOVEL BIPARTITE SPLICING ENHANCER MODULATES THE DIFFERENTIAL PROCESSING OF THE HUMAN FIBRONECTIN EDA EXON
A NOVEL BIPARTITE SPLICING ENHANCER MODULATES THE DIFFERENTIAL PROCESSING OF THE HUMAN FIBRONECTIN EDA EXON
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DOI：
10.1093/nar/22.6.1018
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发表时间：
1994-03-25
影响因子：
14.9
通讯作者：
BARALLE, FE
中科院分区：
文献类型：
--
作者：
CAPUTI, M;CASARI, G;BARALLE, FE
EDA是人纤维连接蛋白的兼性III型同源物，由选择性剪接外显子编码。EDA+和EDA-mRNA呈细胞类型特异性分布，其相对比例在发育、衰老和致癌转化过程中发生变化。我们先前已经证明，外显子本身中的81bp核苷酸序列对于差异RNA的加工是必不可少的。已经对该区域内的顺式作用元件进行了精细定位，以确定可能的靶点以调节选择性剪接。至少涉及两个短核苷酸序列。元件A(GAAGAAGA)是识别外显子的正调控因子，它的缺失会导致EDA外显子的结构性排斥。B元件(CAAGG)是外显子识别的负调制子，它的缺失导致EDA外显子的结构性包涵体。这种剪接增强子的两端结构是哺乳动物外显子的一个新特征。
EDA is a facultative type III homology of human fibronectin encoded by an alternative spliced exon. The EDA+ and EDA- mRNA forms show a cell type specific distribution with their relative proportion varying during development, aging and oncogenic transformation. We have previously demonstrated that an 81 bp nucleotide sequence within the exon itself is essential for differential RNA processing. Fine mapping of cis acting elements within this region has been carried out to identify possible target sites for the modulation of alternative splicing. There are at least two short nucleotide sequences involved. Element A (GAAGAAGA) is a positive modulator for the recognition of the exon, its deletion results in constitutive exclusion of the EDA exon. Element B (CAAGG) is a negative modulator for exon recognition, its deletion results in constitutive inclusion of the EDA exon. This bipartite structure of the splicing enhancer is a novel feature of the mammalian exons.