| Abstract: | Comparison of human and mouse genomics revealed a similar long range sequences organization, and many genes that are orthologous between human and mouse. Alternative splicing is a very important post-transcriptional event leading to an increase in the transcriptome diversity. Recently, genomics studies estimate that 40—60% of human genes undergo alternative splicing. It is interesting to appraise the level of conservation of alternative splicing.
To address this question, we developed a bioinformatics method to identify alternative splicing events that are conserved and alternative splicing events that are not conserved between human and mouse. Here we report an analysis of 3,613 orthologous genes in human and mouse, which discover 2,628 alternative splicing events are conserved in both transcriptome and 2,783 alternative splicing events are not conserved in both transcriptom.
Further classifications of these conserved alternative splicing events reveals that 239 events are due to exon skipping, 34 events is due to mutually exclusive, 1,540 events are due to 3’ splice sites, 815 events are due to 5’ splice sites, and no events are due to intron retention.
By comparison, non-conserved alternative splicing events reveals that 609 events are due to exon skipping, 47 events are due to mutually exclusive, 1,048 events are due to 3’ splice sites, 960 events are due to 5’ splice sites, and 370 events are due to intron retention.
We combined with the human exons and mouse exons to discover the cross-species alternative splicing events. The cross-species alternative splicing events means event that in orthologous genes, there is no alternative splicing event in both species and their splicing forms are distinct. We discovered 235 such events.
We sought to understand the level of expression in conserved alternative splicing events between different species. We have measured the conserved alternative splicing events; major form in one species was also usually major form in other species.
We also tried to find out how the SNPs in human genome affect the non-conservation of alternative splicing (exon skipping) events in mouse. Eleven SNPs in eight genes were identified in human alternative splicing events and may cause non-conservation of such event in mouse. |
