Although introns entail an extra cost in energy and time for DNA replication and transcription, they are abundant in many eukaryotic genomes. This raises the question of the impact of introns on genomic evolution in eukaryotic lineages. Introns might be selfish genetic elements that benefit from the uncoupling of transcription and translation in eukaryotes to invade protein-coding genes. Or, they might confer selective advantages that outweigh the extra cost that they cause. Recently, introns have been proposed to be modifiers of recombination that can reduce the Hill-Robertson effect between exons located in regions of low recombination (Comeron and Kreitman 2000). The Hill-Robertson effect describes the interference between genetically linked loci under selection. Population genetics models predict that, all else being equal, the efficacy of natural selection on nearly neutral mutations should be positively correlated with local recombination rate. In Drosophila melanogaster, larger introns have been found in regions of low recombination. The study of polymorphisms indels revealed that deletion events are more frequent than insertion events in introns of drosophila genes. Thus, selective forces that balance mutational pressure have to be postulated for the maintenance of large introns in the D. melanogaster genome. Theoretical work has shown that neutral or beneficial modifiers that increase recombination between weakly selected loci can be preferentially fixed. Large introns might play the role of such modifiers by spacing exons in regions of low recombination. However, only introns with substantial length are expected to change dramatically the recombination within a gene. If the change in recombination induced by the modifier is small, theorical work showed that the selective effect on this modifier of recombination will be small. Furthermore, analyses on D. melanogaster have been conducted on relatively restricted data sets. Thus, we decided to test the model of Comeron and Kreitman with the complete genomes of D. melanogaster and Caenorhabditis elegans.
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