Abstract
Sequence-based analyses have predicted that ∼35% of mammalian alternative splicing (AS) events produce premature termination codon (PTC)-containing splice variants that are targeted by the process of nonsense-mediated mRNA decay (NMD). This led to speculation that AS may often regulate gene expression by activating NMD. Using AS microarrays, we show that PTC-containing splice variants are generally produced at uniformly low levels across diverse mammalian cells and tissues, independently of the action of NMD. Our results suggest that most PTC-introducing AS events are not under positive selection pressure and therefore may not contribute important functional roles.
Original language | English |
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Pages (from-to) | 153-158 |
Number of pages | 6 |
Journal | Genes and Development |
Volume | 20 |
Issue number | 2 |
DOIs | |
Publication status | Published - 2006 Jan 15 |
Externally published | Yes |
Keywords
- Alternative splicing
- Microarray analysis
- Nonsense-mediated mRNA decay
- Premature termination codon
ASJC Scopus subject areas
- Genetics
- Developmental Biology