Tra2β1 regulates P19 neuronal differentiation and the splicing of FGF-2R and GluR-B minigenes

被引:18
作者
Chen, XH
Huang, J
Li, J
Han, Y
Wu, K
Xu, P
机构
[1] Fudan Univ, Lab Genom Physiol, Shanghai 200433, Peoples R China
[2] Fudan Univ, Ctr Brain Res, Sch Life Sci, State Key Lab Med Neurobiol, Shanghai 200433, Peoples R China
基金
中国国家自然科学基金;
关键词
Tra2; beta; 1; neural differentiation; alternative splicing; FGF-2R minigenes; GluR-B minigenes;
D O I
10.1016/j.cellbi.2004.07.009
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The present study demonstrates that the expression of Tra2beta1 (Transformer 2-beta1) proteins. an SR (serine/arginine rich) protein. is developmentally up-regulated in a neural-specific pattern. The up-regulation is also observed in RA (retinoic acid) induced neural differentiation of P19 cells. Tra2beta1 proteins are located in the nuclei of P19 cells. which are consistent with its functional site as an SR protein. The over-expression of Tra2beta1 proteins promotes RA induced neuronal differentiation of P 19 cells. In P 19 cells. the splicing of FGF-2R (fibroblast growth factor receptor 2) minigene produces the BEK form. while the alternative splicing of GluR-B (glutamate receptor subunit B) minigene generates two products, the Flop and the Truncated isoforms. Tra2beta1 inhibits the BEK splicing, but it promotes the Flop splicing. The results therefore suggest that Tra2beta1 is involved in the regulation of alternative splicing processes during neural development, peculiarly the splicing of FGF-2R and GluR-B genes. Both FGF-2R and GluR-B genes are known to play important roles in neural differentiation. (C) 2004 International Federation for Cell Biology. Published by Elsevier Ltd. All fights reserved.
引用
收藏
页码:791 / 799
页数:9
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