Literature DB >> 25326238

Transcriptome analysis indicates considerable divergence in alternative splicing between duplicated genes in Arabidopsis thaliana.

David C Tack1, William R Pitchers2, Keith L Adams3.   

Abstract

Gene and genome duplication events have created a large number of new genes in plants that can diverge by evolving new expression profiles and functions (neofunctionalization) or dividing extant ones (subfunctionalization). Alternative splicing (AS) generates multiple types of mRNA from a single type of pre-mRNA by differential intron splicing. It can result in new protein isoforms or downregulation of gene expression by transcript decay. Using RNA-seq, we investigated the degree to which alternative splicing patterns are conserved between duplicated genes in Arabidopsis thaliana. Our results revealed that 30% of AS events in α-whole-genome duplicates and 33% of AS events in tandem duplicates are qualitatively conserved within leaf tissue. Loss of ancestral splice forms, as well as asymmetric gain of new splice forms, may account for this divergence. Conserved events had different frequencies, as only 31% of shared AS events in α-whole-genome duplicates and 41% of shared AS events in tandem duplicates had similar frequencies in both paralogs, indicating considerable quantitative divergence. Analysis of published RNA-seq data from nonsense-mediated decay (NMD) mutants indicated that 85% of α-whole-genome duplicates and 89% of tandem duplicates have diverged in their AS-induced NMD. Our results indicate that alternative splicing shows a high degree of divergence between paralogs such that qualitatively conserved alternative splicing events tend to have quantitative divergence. Divergence in AS patterns between duplicates may be a mechanism of regulating expression level divergence.
Copyright © 2014 by the Genetics Society of America.

Entities:  

Keywords:  alternative splicing; gene duplication; genome duplication; genome evolution; nonsense-mediated decay

Mesh:

Substances:

Year:  2014        PMID: 25326238      PMCID: PMC4256766          DOI: 10.1534/genetics.114.169466

Source DB:  PubMed          Journal:  Genetics        ISSN: 0016-6731            Impact factor:   4.562


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