Tra2β1蛋白在神经特异性的基因剪接中的功能

FUNCTION OF TRA2β1 PROTEINS IN THE SPLICING OF NEURAL-SPECIFIC GENES

体外(in vitro)生化研究已证明哺乳动物Tra2蛋白是前体mRNA剪接的重要调控因子,但是,对该蛋白在in vivo条件下的剪接功能,尤其是在神经特异性基因剪接中的功能及其细胞特异性,目前所知甚少。本文采用in vivo分析模型,在COS-1和PFSK两种不同类型的细胞中,研究了两个神经特异性基因(GluR-B,SMN2)剪接的细胞特异性,同时分析了Tra2β1在这两个基因剪接中的功能及其细胞特异性。结果表明,在研究的两种细胞中,GluR-B和SMN2“小基因”的剪接均具有明显的细胞特异性;而Tra2β1蛋白的过量表达在这两种不同的细胞中对“小基因”的剪接有显著的相同倾向的调节作用,提示Tra2β1蛋白对该两个基因剪接的调节作用可能没有细胞特异性。

The in vitro studies have shown that Tra2β1 proteins are important regulators in the alternative pre-mRNA splicing in mammalians. To date, the knowledge regarding the in vivo function of Tra2β1 proteins, especially the function in regulating the splicing of neural-specific genes and the cell-type specificity of the functions is very limited. In the present study, the cell-type specific splicing of two neural-specific genes (GluR-B and SMN2), and the function of Tra2β1 proteins in regulation of the splicing were studied in two types of cells (COS-1 and PFSK-1) using in vivo splicing models. The results showed that the splicing of GluR-B and SMN2 minigenes is cell-type specific, while Tra2β1 proteins regulate the splicing of the minigenes in both cell lines in a similar pattern. It indicates that the Tra2β1 -regulated splicing of GluR-B and SMN2 minigenes regulated by Tra2β1 is not cell-type specific.