Genome-scale comparison of expanded gene families in Plasmodium ovale wallikeri and Plasmodium ovale curtisi with Plasmodium malariae and with other Plasmodium species

Abstract

Malaria in humans is caused by six species of Plasmodium parasites, of which the nuclear genome sequences for the two Plasmodium ovale spp., P. ovale curtisi and P. ovale wallikeri, and Plasmodium malariae have not yet been analyzed. Here we present an analysis of the nuclear genome sequences of these three parasites, and describe gene family expansions therein. Plasmodium ovale curtisi and P. ovale wallikeri are genetically distinct but morphologically indistinguishable and have sympatric ranges through the tropics of Africa, Asia and Oceania. Both P. ovale spp. show expansion of the surfin variant gene family, and an amplification of the Plasmodium interspersed repeat (pir) superfamily which results in an approximately 30% increase in genome size. For comparison, we have also analyzed the draft nuclear genome of P. malariae, a malaria parasite causing mild malaria symptoms with a quartan life cycle, long-term chronic infections, and wide geographic distribution. Plasmodium malariae shows only a moderate level of expansion of pir genes, and unique expansions of a highly diverged transmembrane protein family with over 550 members and the gamete P25/27 gene family. The observed diversity in the P. ovale wallikeri and P. ovale curtisi surface antigens, combined with their phylogenetic separation, supports consideration that the two parasites be given species status.

Plasmodium malariae and Plasmodium ovale infections in the China–Myanmar border area

“…into two distinct subspecies: P. ovale curtisi ( Poc , the classic type) and P. ovale wallikeri ( Pow , the variant type) [12]. The nuclear genome sequences further confirmed that Poc and Pow are genetically distinct but morphologically indistinguishable [13]. Further refinements and applications of the molecular methods have enabled enhanced detection of these parasites in molecular surveillance in endemic countries (e.g., [14–17]) as well as imported cases [18].…”

Tryptophan-rich domains of Plasmodium falciparum SURFIN4.2 and Plasmodium vivax PvSTP2 interact with membrane skeleton of red blood cell

“…As one of the variant surface antigens (VSAs), surfin/pvstp gene family possesses 10 members in P. falciparum and two members in P. vivax ; some were also detected in the genomes of Plasmodium ovale curtisi and Plasmodium ovale wallikeri [14, 16, 38, 39]. Furthermore, previous hierarchical clustering analysis identified two surfin/pvstp genes in Plasmodium gallinaceum ( PgSurf1 and PgSurf2 ), indicating that SURFINs are also conserved outside the human malaria parasites [40].…”

A Feast of Malaria Parasite Genomes

“…Data compiled from Ansari et al (2016) and Rutledge et al (2017). * indicates one or more assemblies generated from culture-adapted or chimpanzee/monkey-adapted strains. …”

“…But multigene families tend to cluster in the repetitive, difficult-to-assemble subtelomeric regions of chromosomes, making it hard to tally gene numbers accurately. Rutledge et al (2017)’s use of long reads using the Pacific Biosciences next-generation sequencing platform, in combination with extensive manual curation, allows them to overcome that common obstacle and upgrade earlier analyses that were based on much lower-quality assemblies (Ansari et al, 2016). They quantitate large differences between P. ovale and P. malariae in gene complements of the pir , STP1 , and surfin families of surface/exported proteins and, most notably, discover two large, previously undistinguished gene families in P. malariae that they relate to a known P. falciparum RBC invasion protein using 3D protein modeling.…”