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    Mol Cell. 2002 Mar;9(3):649-58.

    Dynamic antagonism between ETR-3 and PTB regulates cell type-specific alternative splicing.

    Charlet-B N, Logan P, Singh G, Cooper TA.

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    Department of Pathology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

    Abstract

    Inclusion of cardiac troponin T (cTNT) exon 5 in embryonic muscle requires conserved flanking intronic elements (MSEs). ETR-3, a member of the CELF family, binds U/G motifs in two MSEs and directly activates exon inclusion in vitro. Binding and activation by ETR-3 are directly antagonized by polypyrimidine tract binding protein (PTB). We use dominant-negative mutants to demonstrate that endogenous CELF and PTB activities are required for MSE-dependent activation and repression in muscle and nonmuscle cells, respectively. Combined use of CELF and PTB dominant-negative mutants provides an in vivo demonstration that antagonistic splicing activities exist within the same cells. We conclude that cell-specific regulation results from the dominance of one among actively competing regulatory states rather than modulation of a nonregulated default state.

    PMID:
    11931771
    [PubMed - indexed for MEDLINE]

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