Galiana-Arnoux Delphine, Del Gatto-Konczak Fabienne, Gesnel Marie-Claude, Breathnach Richard
INSERM U601, Institut de Biologie-CHR, 9 quai Moncousu, 44093 Nantes Cedex 1, France.
Biochem Biophys Res Commun. 2005 Oct 21;336(2):667-73. doi: 10.1016/j.bbrc.2005.08.153.
Alternative CD44 exons v8, v9, and v10 are spliced as a block in epithelial cells (for example SVK14 cells), but can be skipped as a block by other cells. Using a minigene approach, we show that downstream intronic UGG repeats participate in activation of v8 exon splicing in SVK14 cells. The repeats can activate splicing of a heterologous exon in SVK14 cells and act additively with a previously described v8 exon splicing enhancer in this context. An alternative v9 exon 5' splice site used by some cells to make an aberrant transcript is repressed by an immediately downstream (UGG)3 sequence in SVK14 cells. We conclude that UGG repeats both activate v8 exon splicing and repress use of the alternative v9 exon 5' splice site in SVK14 cells, thus participating in the coordination of correct epithelial cell splicing of the v8-10 block.
可变剪接的CD44外显子v8、v9和v10在上皮细胞（如SVK14细胞）中作为一个整体进行剪接，但在其他细胞中可作为一个整体被跳过。通过小基因方法，我们发现下游内含子中的UGG重复序列参与了SVK14细胞中v8外显子剪接的激活。这些重复序列可激活SVK14细胞中异源外显子的剪接，并在这种情况下与先前描述的v8外显子剪接增强子协同作用。一些细胞用于产生异常转录本的可变v9外显子5'剪接位点在SVK14细胞中被紧邻下游的(UGG)3序列所抑制。我们得出结论，UGG重复序列既激活了SVK14细胞中v8外显子的剪接，又抑制了可变v9外显子5'剪接位点的使用，从而参与了v8-10片段在上皮细胞中正确剪接的协调过程。
