Evolution of the merozoite surface protein 7 (msp7) family in Plasmodium vivax and P. falciparum: A comparative approach.
Malaria parasites (genus Plasmodium) are a diverse group found in many species of vertebrate hosts. These parasites invade red blood cells in a complex process comprising several proteins, many encoded by multigene families, one of which is merozoite surface protein 7 (msp7). In the case of Plasmodium vivax, the most geographically widespread human-infecting species, differences in the number of paralogs within multigene families have been previously explained, at least in part, as potential adaptations to the human host. To explore this in msp7, we studied its orthologs in closely related nonhuman primate parasites; investigating both paralog evolutionary history and genetic polymorphism. The emerging patterns were then compared with the human parasite Plasmodium falciparum. We found that the evolution of the msp7 family is consistent with a birth-and-death model, where duplications, pseudogenizations, and gene loss events are common. However, all paralogs in P. vivax and P. falciparum had orthologs in their closely related species in non-human primates indicating that the ancestors of those paralogs precede the events leading to their origins as human parasites. Thus, the number of paralogs cannot be explained as an adaptation to human hosts. Although there is no functional information for msp7 in P. vivax, we found evidence for purifying selection in the genetic polymorphism of some of its paralogs as well as their orthologs in closely related non-human primate parasites. We also found evidence indicating that a few of P. vivax's paralogs may have diverged from their orthologs in non-human primates by episodic positive selection. Hence, they may had been under selection when the lineage leading to P. vivax diverged from the Asian non-human primates and switched into Homininae. All these lines of evidence suggest that msp7 is functionally important in P. vivax.
Arizona State University, School of Life Sciences, Tempe, AZ, USA.
Andreína I
AI
Castillo
Department of Biology, Institute for Genomics and Evolutionary Medicine (igem), Temple University, Philadelphia, PA, USA.
M
M
Andreína Pacheco
Department of Biology, Institute for Genomics and Evolutionary Medicine (igem), Temple University, Philadelphia, PA, USA. Electronic address: Ananias.Escalante@temple.edu.
Ananias A
AA
Escalante
D000595:Amino Acid Sequence; D000818:Animals; D004912:Erythrocytes / Q000469:parasitology; D019143:Evolution, Molecular; D017353:Gene Deletion; D020440:Gene Duplication; D015870:Gene Expression; D049810:Genetic Speciation; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics*; D008957:Models, Genetic; D005810:Multigene Family; D010802:Phylogeny; D016789:Plasmodium cynomolgi / Q000145:classification / Q000235:genetics*; D010963:Plasmodium falciparum / Q000145:classification / Q000235:genetics*; D016790:Plasmodium knowlesi / Q000145:classification / Q000235:genetics*; D010966:Plasmodium vivax / Q000145:classification / Q000235:genetics*; D011110:Polymorphism, Genetic; D011323:Primates / Q000469:parasitology; D015800:Protozoan Proteins / Q000235:genetics*; D011544:Pseudogenes; D012641:Selection, Genetic; D017386:Sequence Homology, Amino Acid
D008565:Membrane Proteins; D015800:Protozoan Proteins; C439571:merozoite surface protein 7, Plasmodium
Episodic positive selection; Merozoite surface proteins 7; Multigene family; Plasmodium falciparum; Plasmodium vivax; Pseudogenization