Selection shapes malaria genomes and drives divergence between pathogens infecting hominids versus rodents
1 Laboratoire GEMI, UMR 2724 CNRS-IRD, 911 avenue Agropolis, BP 64501, 34394 Montpellier Cedex 5, France
2 Department of Genetics, North Carolina State University, PO Box 7614, Raleigh 27659, USA
3 Ste Justine Hospital Research Centre, Department of Pediatric, Faculty of Medicine, University of Montreal, Montreal H3T 1C5, Canada
BMC Evolutionary Biology 2008, 8:223 doi:10.1186/1471-2148-8-223Published: 30 July 2008
Malaria kills more people worldwide than all inherited human genetic disorders combined. To characterize how the parasites causing this disease adapt to different host environments, we compared the evolutionary genomics of two distinct groups of malaria pathogens in order to identify critical properties associated with infection of different hosts: those parasites infecting hominids (Plasmodium falciparum and P. reichenowi) versus parasites infecting rodent hosts (P. yoelii yoelii, P. berghei, and P. chabaudi). Adaptation by the parasite to its host is likely highly critical to the evolution of these species.
Our comparative analysis suggests that patterns of molecular evolution in the hominid parasite lineage are generally similar to those of the rodent lineage but distinct in several aspects. The most rapidly evolving genes in both lineages are those involved in host-parasite interactions as well as those that show the lowest expression levels. However, we found that, similar to their respective mammal host lineages, parasite genomes infecting hominids are generally less constrained, evolving at faster rates, and accumulating more deleterious mutations than those infecting murids, which may reflect an historical lower effective size of the hominid lineage and relaxed host-driven selective pressures.
Our study highlights for the first time the differences in trends and rates of evolution in Plasmodium lineages infecting different hosts and emphasizes the potential importance of the variation in effective size between lineages to explain variation in selective constraints among genomes.