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A splicing silencer that regulates smooth muscle specific alternative splicing is active in multiple cell types.
Nucleic Acids Res. 2002 Aug 15; 30(16):3548-57.NA

Abstract

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.

Authors+Show Affiliations

Department of Biochemistry, University of Cambridge, 80 Tennis Court Road, Cambridge CB2 1GA, UK.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12177296

Citation

Gromak, Natalia, and Christopher W J. Smith. "A Splicing Silencer That Regulates Smooth Muscle Specific Alternative Splicing Is Active in Multiple Cell Types." Nucleic Acids Research, vol. 30, no. 16, 2002, pp. 3548-57.
Gromak N, Smith CW. A splicing silencer that regulates smooth muscle specific alternative splicing is active in multiple cell types. Nucleic Acids Res. 2002;30(16):3548-57.
Gromak, N., & Smith, C. W. (2002). A splicing silencer that regulates smooth muscle specific alternative splicing is active in multiple cell types. Nucleic Acids Research, 30(16), 3548-57.
Gromak N, Smith CW. A Splicing Silencer That Regulates Smooth Muscle Specific Alternative Splicing Is Active in Multiple Cell Types. Nucleic Acids Res. 2002 Aug 15;30(16):3548-57. PubMed PMID: 12177296.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A splicing silencer that regulates smooth muscle specific alternative splicing is active in multiple cell types. AU - Gromak,Natalia, AU - Smith,Christopher W J, PY - 2002/8/15/pubmed PY - 2002/10/2/medline PY - 2002/8/15/entrez SP - 3548 EP - 57 JF - Nucleic acids research JO - Nucleic Acids Res VL - 30 IS - 16 N2 - 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. SN - 1362-4962 UR - https://www.unboundmedicine.com/medline/citation/12177296/A_splicing_silencer_that_regulates_smooth_muscle_specific_alternative_splicing_is_active_in_multiple_cell_types_ L2 - https://academic.oup.com/nar/article-lookup/doi/10.1093/nar/gkf480 DB - PRIME DP - Unbound Medicine ER -