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Alternative splicing of fibronectin mRNAs in chondrosarcoma cells: Role of far upstream intron sequences
Journal article   Peer reviewed

Alternative splicing of fibronectin mRNAs in chondrosarcoma cells: Role of far upstream intron sequences

Matthew Flanagan, Hongyan Liang and Pamela A Norton
Journal of cellular biochemistry, v 90(4), pp 709-718
01 Nov 2003
DOI: https://doi.org/10.1002/jcb.10687
PMID: 14587027
Featured in Collection :   UN Sustainable Development Goals @ Drexel

Abstract

intronic splicing enhancer mRNA splicing extracellular matrix PTB
The fibronectin (FN) gene encodes multiple mRNAs through the process of alternative splicing, and production of certain isoforms is characteristic of a given cell type. Chondrocytes produce FNs that completely lack alternative exon EIIIA, and loss of inclusion of the exon is tightly linked to chondrogenic condensation of mesenchymal cells. The inclusion of a second exon, EIIIB, is high in embryonic cartilage, but declines with age. Multiple exons are omitted to produce the (V + C)‐form that is highly specific for cartilage and chondrocytes. A rat chondrosarcoma cell line, RCS, was identified that preserves key features of the cartilage‐specific splicing phenotype. RCS cells, which exclude exon EIIIA, and HeLa cells, which include exon EIIIA similar to mesenchymal cells, were used to assess the contribution of intron sequences flanking exon EIIIA to splicing regulation. Deletion of most of the intron downstream of the exon had little effect on splicing in either cell type. However, deletions within upstream intron 32‐A reduced inclusion of the alternative exon in both cell types. The sequences involved lie more than 200 nucleotides away from the exon, but could not be localized to a single region by deletion mapping. These intronic sequences contribute to the efficiency of exon EIIIA recognition, but not to cell‐type specific regulation. The normally inhibitory factor polypyrimidine tract binding protein promotes exon EIIIA inclusion in a manner that is partially dependent on the regulatory sequences within intron 32‐A. © 2003 Wiley‐Liss, Inc.

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Web of Science research areas
Biochemistry & Molecular Biology
Cell Biology
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