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Updated: May 30, 2026
11:48
Detection of Alternative Splicing During Epithelial-Mesenchymal Transition
Published on: October 9, 2014
Increased complexity of Tmem16a/Anoctamin 1 transcript alternative splicing.
Kate E O'Driscoll1, Rachel A Pipe, Fiona C Britton
1Department of Physiology and Cell Biology, 1664 North Virginia Street, University of Nevada School of Medicine, Reno, Nevada 89557-0046, USA.
BMC Molecular Biology
|August 10, 2011
Summary
The mouse Tmem16a gene exhibits more alternative splicing than previously known, generating diverse calcium-activated chloride channel variants. These splicing events are conserved in humans and impact channel function.
Area of Science:
- Molecular Biology
- Genomics
- Ion Channel Physiology
Background:
- TMEM16A (Anoctamin 1; ANO1) is a crucial calcium-activated chloride channel protein.
- Human TMEM16A has alternatively spliced exons (6b, 13, 15) regulating channel function.
- Mouse Tmem16a has 25 exons encoding a 956 amino acid protein.
Purpose of the Study:
- To detail the genomic structure of mouse Tmem16a.
- To investigate alternative splicing in mouse Tmem16a transcripts.
- To explore the generation of channel diversity through splicing.
Main Methods:
- Genomic structure analysis of mouse Tmem16a.
- Transcript variant identification using sequencing.
- Expression analysis in various mouse tissues.
Main Results:
- Identified Tmem16a transcript variants with alternative exons (6b, 10, 13, 14, 15, 18).
- Observed conserved splicing patterns between mouse and human.
- Discovered novel exon 13b, tandem splice sites, and intron retention events.
Conclusions:
- Mouse Tmem16a gene exhibits greater complexity than previously understood.
- Alternative splicing significantly diversifies TMEM16A channel function.
- Splicing events, particularly in exons 6-16, affect channel properties like calcium sensitivity and kinetics.
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