Evolution of alternative splicing after gene duplication (original) (raw)

  1. Zhixi Su1,2,6,
  2. Jianmin Wang3,6,
  3. Jun Yu1,5,
  4. Xiaoqiu Huang3,4, and
  5. Xun Gu1,2,4,7
  6. 1 James D. Watson Institute of Genome Sciences, Zhejiang University, Hangzhou 310008, China
  7. 2 Department of Genetics, Development, and Cell Biology, Iowa State University, Ames, Iowa 50011, USA
  8. 3 Department of Computer Science, and Iowa State University, Ames, Iowa 50011, USA
  9. 4 Departments of Center for Bioinformatics and Biological Statistics, Iowa State University, Ames, Iowa 50011, USA
  10. 5 Beijing Genomics Institute, Chinese Academy of Sciences, Beijing 101300, China

Abstract

Alternative splicing and gene duplication are two major sources of proteomic function diversity. Here, we study the evolutionary trend of alternative splicing after gene duplication by analyzing the alternative splicing differences between duplicate genes. We observed that duplicate genes have fewer alternative splice (AS) forms than single-copy genes, and that a negative correlation exists between the mean number of AS forms and the gene family size. Interestingly, we found that the loss of alternative splicing in duplicate genes may occur shortly after the gene duplication. These results support the subfunctionization model of alternative splicing in the early stage after gene duplication. Further analysis of the alternative splicing distribution in human duplicate pairs showed the asymmetric evolution of alternative splicing after gene duplications; i.e., the AS forms between duplicates may differ dramatically. We therefore conclude that alternative splicing and gene duplication may not evolve independently. In the early stage after gene duplication, young duplicates may take over a certain amount of protein function diversity that previously was carried out by the alternative splicing mechanism. In the late stage, the gain and loss of alternative splicing seem to be independent between duplicates.

Footnotes