Abstract
BackgroundThe human malaria parasite Plasmodium falciparum survives pressures from the host immune system and antimalarial drugs by modifying its genome. Genetic recombination and nucleotide substitution are the two major mechanisms that the parasite employs to generate genome diversity. A better understanding of these mechanisms may provide important information for studying parasite evolution, immune evasion and drug resistance.ResultsHere, we used a high-density tiling array to estimate the genetic recombination rate among 32 progeny of a P. falciparum genetic cross (7G8 × GB4). We detected 638 recombination events and constructed a high-resolution genetic map. Comparing genetic and physical maps, we obtained an overall recombination rate of 9.6 kb per centimorgan and identified 54 candidate recombination hotspots. Similar to centromeres in other organisms, the sequences of P. falciparum centromeres are found in chromosome regions largely devoid of recombination activity. Motifs enriched in hotspots were also identified, including a 12-bp G/C-rich motif with 3-bp periodicity that may interact with a protein containing 11 predicted zinc finger arrays.ConclusionsThese results show that the P. falciparum genome has a high recombination rate, although it also follows the overall rule of meiosis in eukaryotes with an average of approximately one crossover per chromosome per meiosis. GC-rich repetitive motifs identified in the hotspot sequences may play a role in the high recombination rate observed. The lack of recombination activity in centromeric regions is consistent with the observations of reduced recombination near the centromeres of other organisms.
Highlights
The human malaria parasite Plasmodium falciparum survives pressures from the host immune system and antimalarial drugs by modifying its genome
Single feature polymorphism detection and genotype verification Applying the single-feature polymorphism (SFP) calling parameters described previously [10], we identified 5,672 putative SFPs that differed between the GB4 and 3D7 parasites, 11,892 putative SFPs that differed between 7G8 and 3D7, and 9,030 putative SFPs that were the same between GB4 and 7G8 but differed from 3D7
Potential errors in genotype calls were corrected using the procedures described in Materials and methods, leading to 3,184 high-quality multiprobe SFP (mSFP) (Table 1)
Summary
The human malaria parasite Plasmodium falciparum survives pressures from the host immune system and antimalarial drugs by modifying its genome. Genetic recombination and nucleotide substitution are the two major mechanisms that the parasite employs to generate genome diversity. The human malaria parasite Plasmodium falciparum kills approximately one million people each year, mostly children in Africa [1]. Parasite resistance to multiple antimalarial drugs has spread rapidly in recent years. Genome plasticity and genetic variation are significant challenges to vaccine development and contribute to the worldwide problem of drug resistance. The P. falciparum malaria parasite has a unique and complex life cycle involving multiple DNA replications cycle produces millions of haploid asexual parasites, a small proportion of the parasites differentiates into male and female sexual stages - termed gametocytes - that circulate in the bloodstream. Completion of the life cycle offers many opportunities for genetic recombination and mutation events during numerous rounds of DNA replication
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