Abstract
The genome sequences of the neglected human-infective malaria species Plasmodium malariae and P. ovale provide new insights into their biology that are pertinent to understanding their epidemiology and to the broader agenda of malaria elimination.
Highlights
Elucidation of the evolutionary history and interrelatedness of Plasmodium species that infect humans has been hampered by a lack of genetic information for three human-infective species: P. malariae and two P. ovale species (P. o. curtisi and P. o. wallikeri)[1]
Additional draft genomes for both species of P. ovale were assembled from P. falciparum co-infections and the genome of a parasite that we call ‘P. malariae-like’ was assembled from a chimpanzee co-infected with P. reichenowi (Fig. 1; Table 1; Extended Data Table 2; Supplementary Information)
Using additional samples to calculate standard measures of molecular evolution (Methods; Supplementary Information), we identified a subset of genes under selection in both P. malariae and P. malariae-like and in an earlier study of P. falciparum and P. reichenowi[10] (Extended Data Fig. 3a; Extended Data Table 3), showing some conservation of selection pressures in Plasmodium lineages and suggesting host- specific adaptation of parasites to human and chimpanzee hosts
Summary
Contrasts with other previous studies[1,7,11] (Supplementary Information). our phylogenetic analysis is based on the most comprehensive amino acid alignment to date, which is enriched for neutrally evolving sites through stringent filtering and has been subjected to a number of different sensitivity tests (Supplementary Information). Assuming consistent mutation rates and generation times across the branches (Supplementary Information), we find that the relative split between the two P. ovale species is about five times earlier than the split between P. falciparum and P. reichenowi, whereas P. malariae and P. malariae-like seem to have split at a similar time to the latter two (Fig. 2). Manual curation of about 5,000 gene models of both P. malariae and P. o. Curtisi enabled a detailed exploration of lineage-specific differences in gene content (Table 1), with some paralogous expansions being notable (Extended Data Fig. 1c, d). The manual curation enabled pseudogenes that are differentially distributed between the two genomes and other human-infective Plasmodium species (Extended Data Table 5) to be analysed in ways not possible using computer- annotated draft genome data[7]. Pseudogenes are found among a paralogously expanded family of invasion-associated RBPs (Extended Data Fig. 4a–e), and a homologue of a P. falciparum cyclin (PF3D7_1227500) is only pseudogenized in P. o. Pseudogenes are found among a paralogously expanded family of invasion-associated RBPs (Extended Data Fig. 4a–e), and a homologue of a P. falciparum cyclin (PF3D7_1227500) is only pseudogenized in P. o. wallikeri and may
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