title: Tra2betal regulates P19 neuronal differentiation and the splicing of FGF-2R and GluR-B minigenes.
abstract: 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. Tra2betal proteins are located in the nuclei of P19 cells, which are consistent with its functional site as an SR protein. The over-expression of Tra2betal 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. Tra2betal inhibits the BEK splicing, but it promotes the Flop splicing. The results therefore suggest that Tra2betal 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.
authors.affiliation: Laboratory of Genomic Physiology and Center for Brain Research, School of Life Sciences, State Key Laboratory of Medical Neurobiology, Fudan University, 220 Handan Road, Shanghai, 200433, People's Republic of China.
authors.forename: Xianhua
authors.initials: X
authors.lastname: Chen
authors.forename: Jia
authors.initials: J
authors.lastname: Huang
authors.forename: Jing
authors.initials: J
authors.lastname: Li
authors.forename: Yu
authors.initials: Y
authors.lastname: Han
authors.forename: Kun
authors.initials: K
authors.lastname: Wu
authors.forename: Ping
authors.initials: P
authors.lastname: Xu
mesh_terms: D017398:Alternative Splicing / Q000187:drug effects*; D000818:Animals; D000831:Animals, Newborn; D002454:Cell Differentiation / Q000187:drug effects*; D018507:Gene Expression Regulation, Developmental; D051379:Mice; D008807:Mice, Inbred BALB C / Q000196:embryology; D009474:Neurons / Q000166:cytology* / Q000378:metabolism; D009687:Nuclear Proteins; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D012322:RNA Precursors / Q000235:genetics / Q000378:metabolism; D012326:RNA Splicing; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000235:genetics / Q000494:pharmacology*; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics* / Q000378:metabolism; D051497:Receptor, Fibroblast Growth Factor, Type 2; D018091:Receptors, AMPA / Q000235:genetics* / Q000378:metabolism; D017468:Receptors, Fibroblast Growth Factor / Q000235:genetics* / Q000378:metabolism; D000068103:Serine-Arginine Splicing Factors; D014212:Tretinoin / Q000494:pharmacology; D014407:Tumor Cells, Cultured; D015854:Up-Regulation
chemical_list: D009687:Nuclear Proteins; D020033:Protein Isoforms; D012322:RNA Precursors; D012333:RNA, Messenger; D016601:RNA-Binding Proteins; D018091:Receptors, AMPA; D017468:Receptors, Fibroblast Growth Factor; C100345:Tra2b protein, mouse; C115953:glutamate receptor type B; D000068103:Serine-Arginine Splicing Factors; D014212:Tretinoin; C496354:Fgfr2 protein, mouse; D020794:Receptor Protein-Tyrosine Kinases; D051497:Receptor, Fibroblast Growth Factor, Type 2