期刊
RNA
卷 9, 期 4, 页码 443-456出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1261/rna.2191903
关键词
polypyrimidine tract binding protein; PTB; CUG-BP; bruno-like proteins; hnRNP
资金
- NHLBI NIH HHS [R01 HL045565, HL45565] Funding Source: Medline
The alpha-actinin gene has a pair of alternatively spliced exons. The smooth muscle (SM) exon is repressed in most cell types by polypyrimidine tract binding protein (PTB). CELF ((C) under bar UG-BP and (E) under bar TR3-(l) under bar ike (f) under bar actors) family proteins, splicing regulators whose activities are altered in myotonic dystrophy, were found to coordinately regulate selection of the two alpha-actinin exons. CUG-BP and ETR3 activated the SM exon, and along with CELF4 they were also able to repress splicing of the NM (nonmuscle) exon both in vivo and in vitro. Activation of SM exon splicing was associated with displacement of PTB from the polypyrimidine tract by binding of CUG-BP at adjacent sites. Our data provides direct evidence for the activity of CELF proteins as both activators and repressors of splicing within a single-model system of alternative splicing, and suggests a model whereby a-actinin alternative splicing is regulated by synergistic and antagonistic interactions between members of the CELF and PTB families.
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