Abstract
Gene duplication and alternative splicing are distinct evolutionary mechanisms that provide the raw material for new biological functions. We explored their relationships in human and mouse and found an inverse correlation between the size of a gene's family and its use of alternatively spliced isoforms. A cross-organism analysis suggests that selection for genome-wide genic proliferation might be interchangeably met by either evolutionary mechanism.
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Acknowledgements
We thank A. Derti for a critical reading of the manuscript and Y. Groner, E. Domany, M.J. Lercher, A. Bar-Even and S.J. Fleishman for discussions. I.Y. is a Koshland Scholar and D.L. is the incumbent of the Ralph and Lois Silver Chair in Human Genomics. This research is supported by the Crown Human Genome Center, the Abraham and Judith Goldwasser Foundation and the Koshland Center for Basic Research.
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Supplementary information
Supplementary Fig. 1
Independence of relationship with respect to binning. (PDF 95 kb)
Supplementary Fig. 2
Independence of relationship to the number of exons. (PDF 41 kb)
Supplementary Fig. 3
Independence of inverse relationship on the coverage of EST counts per exon. (PDF 92 kb)
Supplementary Fig. 4
Inverse relationship shown on a gene family basis. (PDF 35 kb)
Supplementary Fig. 5
Results for Ensembl delineation of orthologous families. (PDF 54 kb)
Supplementary Fig. 6
Independent estimation of isoform count. (PDF 37 kb)
Supplementary Table 1
Independence of relationship to the number of exons. (PDF 121 kb)
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Kopelman, N., Lancet, D. & Yanai, I. Alternative splicing and gene duplication are inversely correlated evolutionary mechanisms. Nat Genet 37, 588–589 (2005). https://doi.org/10.1038/ng1575
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DOI: https://doi.org/10.1038/ng1575
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