4.8 Article

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

Journal

MOLECULAR CELL
Volume 9, Issue 3, Pages 649-658

Publisher

CELL PRESS
DOI: 10.1016/S1097-2765(02)00479-3

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Funding

  1. NHLBI NIH HHS [R01HL45565] Funding Source: Medline
  2. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL045565] Funding Source: NIH RePORTER

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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.

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