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Alternative splicing of alpha-tropomyosin (alpha-TM) involves mutually exclusive selection of exons 2 and 3. Selection of exon 2 in smooth muscle (SM) cells is due to inhibition of exon 3, which requires both binding sites for polypyrimidine tract-binding protein as well as UGC (or CUG) repeat elements on both sides of exon 3. Point mutations or substitutions of the UGC-containing upstream regulatory element (URE) with other UGC elements disrupted the alpha-TM splicing pattern in transfected cells. Multimerisation of the URE caused enhanced exon skipping in SM and various non-SM cells. In the presence of multiple UREs the degree of splicing regulation was decreased due to the high levels of exon skipping in non-SM cell lines. These results suggest that the URE is not an intrinsically SM- specific element, but that its functional strength is fine tuned to exploit differences in the activities of regulatory factors between SM and other cell types. Co-transfection of tropomyosin reporters with members of the CUG-binding protein family, which are candidate URE-binding proteins, indicated that these factors do not mediate repression of tropomyosin exon 3.


Journal article


Nucleic Acids Res

Publication Date





3548 - 3557


Alternative Splicing, Animals, Base Sequence, CCAAT-Enhancer-Binding Protein-delta, CCAAT-Enhancer-Binding Proteins, Cell Line, Exons, Humans, Mice, Molecular Sequence Data, Muscle, Smooth, Mutation, Organ Specificity, RNA Precursors, RNA, Messenger, Rats, Regulatory Sequences, Nucleic Acid, Response Elements, Transcription Factors, Tropomyosin