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- W3173685877 abstract "Recently, it was proposed that alternative splicing may act as a mechanism for opening accelerated paths of evolution, by reducing negative selection pressure against large-scale alterations of gene structure such as exon creation or loss. This hypothesis raises a number of questions. First, has this mechanism actually created new exons in mammalian genomes? The original analysis showed that many alternatively spliced exons are species-specific (i.e. present in the human genome but not mouse, or vice versa), but assessing whether this is due to recent exon creation (as opposed to exon loss) requires using outgroups to infer the ancestral genotype (i.e. whether the exon was present or absent in the common ancestor). Second, has neutralization of negative selection by alternative splicing produced actual adaptive benefit during mammalian evolution? How can we assess whether alternatively spliced exons show both evidence of “faster evolution” than other exons, and at the same time strong selection pressure that is indicative of biological function? Third, protein reading frame-preservation (alternative splicing that adds or removes an exact multiple of 3nt to the transcript, altering the protein sequence in a strictly modular way) has emerged as an important criterion for functional alternative splicing. What is the evolutionary role of such “modular” alternative splicing events, and what distinguishes them from other alternative splicing? We will discuss our recent studies on these problems." @default.
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- W3173685877 date "2006-03-01" @default.
- W3173685877 modified "2023-09-23" @default.
- W3173685877 title "How alternative splicing helped build the genome: exon creation, locally accelerated sequence evolution, and the production of new tissue‐specific functions." @default.
- W3173685877 doi "https://doi.org/10.1096/fasebj.20.4.a61-c" @default.
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