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Tra2βl regulates P19 neuronal differentiation and the splicing of FGF‐2R and GluR‐B minigenes
Author(s) -
Chen Xianhua,
Huang Jia,
Li Jing,
Han Yu,
Wu Kun,
Xu Ping
Publication year - 2004
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/j.cellbi.2004.07.009
Subject(s) - minigene , rna splicing , sr protein , alternative splicing , microbiology and biotechnology , biology , exonic splicing enhancer , fibroblast growth factor , p19 cell , gene isoform , cellular differentiation , receptor , gene , genetics , rna , adult stem cell
The present study demonstrates that the expression of Tra2β1 (Transformer 2‐β1) 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. Tra2βl proteins are located in the nuclei of P19 cells, which are consistent with its functional site as an SR protein. The over‐expression of Tra2βl proteins promotes RA induced neuronal differentiation of P19 cells. In P19 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. Tra2βl inhibits the BEK splicing, but it promotes the Flop splicing. The results therefore suggest that Tra2βl 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.