NSSR1 promotes neuronal differentiation of mouse embryonic carcinoma P19 cells

• Published in: Neuroreport Vol. 15; no. 5; p. 823
• Main Authors: Liu, Lei, Chen, Xian-hua, Huang, Jia, Lin, Jun-ji, Lin, Wan-min, Xu, Ping
• Format: Journal Article
• Language: English
• Published: England 09.04.2004
• Subjects: Alternative Splicing; Animals; Blotting, Northern - methods; Blotting, Western - methods; Bromodeoxyuridine - metabolism; Carcinoma; Carrier Proteins - physiology; Cell Count; Cell Cycle Proteins; Cell Differentiation - physiology; Cell Line, Tumor; Embryo, Mammalian; Exons; Gene Expression - drug effects; Gene Expression Regulation; Mice; Neoplasm Proteins - physiology; Neural Cell Adhesion Molecules - genetics; Neural Cell Adhesion Molecules - metabolism; Neurons - pathology; Receptor, trkC - genetics; Receptor, trkC - metabolism; Receptors, GABA-A - genetics; Receptors, GABA-A - metabolism; Repressor Proteins - physiology; Reverse Transcriptase Polymerase Chain Reaction - methods; RNA, Messenger - biosynthesis; RNA, Small Interfering - pharmacology; RNA-Binding Proteins - physiology; Transfection - methods; Tubulin - metabolism
• ISSN: 0959-4965
• DOI: 10.1097/00001756-200404090-00017

We generated the small interference RNAs to specifically silence the expression of neural salient serine/arginine rich protein 1 (NSSR1) and showed that the inhibition of NSSR1 expression in mouse embryonic carcinoma cells (P19) reduces neuronal differentiation. By contrast, its over-expression promotes the differentiation. Neither inhibition nor over-expression shows distinct effect on cell proliferation. The over-expression increases the inclusion of NCAM L1 exon2 while the inhibition reduces the inclusion. The splicing of kinase insert free isoform of TrkC (TrkC-K1) is increased by the over-expression. The results demonstrate that NSSR1 promotes neuronal differentiation and the splicing of NCAML1 exon2 and TrkC-K1.