Leslie Turner’s research focuses on identifying and functionally characterizing genes contributing to speciation in rodents. Bettina Harr is using the house mouse as model to study divergence and speciation at the molecular level.
Genome-wide analysis of alternative splicing evolution among Mus subspecies
Article first published online: 10 FEB 2010
© 2010 Blackwell Publishing Ltd
Special Issue: Next Generation Molecular Ecology
Volume 19, Issue Supplement s1, pages 228–239, March 2010
How to Cite
HARR, B. and TURNER, L. M. (2010), Genome-wide analysis of alternative splicing evolution among Mus subspecies. Molecular Ecology, 19: 228–239. doi: 10.1111/j.1365-294X.2009.04490.x
- Issue published online: 10 FEB 2010
- Article first published online: 10 FEB 2010
- Received 21 June 2009; revision received 13 October 2009; accepted 30 October 2009
- alternative splicing;
- house mouse;
Alternative splicing, the combination of different exons to produce a variety of transcripts from a single gene, contributes enormously to transcriptome diversity in mammals, and the majority of genes encode alternatively spliced products. Previous research comparing mouse, rat and human has shown that a significant proportion of splice forms are not conserved across species, suggesting that alternative transcripts are an important source of evolutionary novelty. Here, we studied the evolution of alternative splicing in the early stages of species divergence in the house mouse. We sequenced the testis transcriptomes of three Mus musculus subspecies and Mus spretus using Illumina technology. On the basis of a genome-wide analysis of read coverage differences among subspecies, we identified several hundred candidate alternatively spliced regions. We conservatively estimate that 6.5% of testis-expressed genes show alternative splice differences between at least one pair of M. musculus subspecies, a proportion slightly higher than the proportion of genes differentially expressed among subspecies. These results suggest that differences in both the structure and abundance of transcripts contribute to early transcriptome divergence.