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MBE Advance Access published online on April 14, 2004

Molecular Biology and Evolution, doi:10.1093/molbev/msh143
Molecular Biology and Evolution © Society for Molecular Biology and Evolution 2004; all rights reserved
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Accepted March 22, 2004

Original Articles

Accelerated Rates of Intron Gain/Loss and Protein Evolution in Duplicate Genes in Human and Mouse Malaria Parasites

Cristian I. Castillo-Davis 1, Trevor B. C. Bedford 1, Daniel L. Hartl 1*

1 Department of Organismic and Evolutionary Biology, Harvard University, Cambridge, MA 02138 USA

* To whom correspondence should be addressed. E-mail: dhartl{at}oeb.harvard.edu.


   Abstract

Very little is known about molecular evolution in the human malaria parasite P. falciparum. Given the potentially important role that introns play in directing transcription and the post-transcriptional control of gene expression, we compare rates of intron gain/loss and intronic substitution in P. falciparum and the rodent malaria P. y. yoelii in both orthologous and duplicate genes. Specifically, we test the hypothesis that intron gain/loss and protein evolution is accelerated in duplicate genes versus orthologous genes in both parasites using the genome sequence of both species. We find that duplicate genes in both P. falciparum and P. y. yoelii exhibit a dramatic acceleration of both intron gain/loss and protein evolution in comparison with orthologs, suggesting increased directional and/or relaxed selection in duplicate genes. Further, we find that rates of intron gain/loss and protein evolution are weakly coupled in orthologs but not paralogs, supporting the hypothesis that selection acts on genes as functionally integrated units following speciation but not necessarily gene duplication. In contrast, we find that rates of nucleotide substitution do not differ significantly between intronic sites and synonymous sites among duplicate genes, implying that a large fraction of intronic sites in Plasmodium evolve under little or no selective constraint.

Key Words: gene duplication, genome evolution, intron gain/loss, malaria


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