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As well as generating protein isoform diversity, in some cases alternative splicing generates RNAs that harbor premature termination codons and that are subject to nonsense-mediated decay (NMD). We previously identified an apparent pseudo-exon in the rat alpha-tropomyosin (Tpm1) gene as a probable genuine alternatively spliced exon that causes NMD when spliced into Tpm1 RNA. Here, we report the analysis of cis-acting splicing regulatory elements within this "nonsense exon." Guided by the data set of predicted splicing enhancer and silencer elements compiled by Zhang and Chasin, we made a series of mutations through the nonsense exon and found that like authentic exons it is densely packed with enhancer and silencer elements. Strikingly, 11 of 13 tested mutations behaved as predicted computationally. In particular, we found that a G-rich silencer at the 5' end, which is crucial for skipping of the nonsense exon, functions by binding hnRNP-H and F.

Original publication

DOI

10.1261/rna.1225209

Type

Journal article

Journal

RNA

Publication Date

01/2009

Volume

15

Pages

33 - 43

Keywords

Alternative Splicing, Animals, Base Sequence, Codon, Nonsense, Enhancer Elements, Genetic, Exons, Gene Silencing, HeLa Cells, Heterogeneous-Nuclear Ribonucleoprotein Group F-H, Humans, Molecular Sequence Data, RNA Precursors, Rats, Tropomyosin