![]() ![]() Completion of the life cycle therefore offers many opportunities for genetic recombination and mutation events during numerous rounds of DNA replication. The motile ookinete subsequently develops into an oocyst containing thousands of sporozoites after rounds of mitotic divisions. When the gametocytes are taken up by a feeding mosquito during a blood meal, they develop into male and female gametes, mate, and form a diploid zygote that develops into an ookinete genetic recombination and meiosis occur at this time. While the erythrocytic 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. This erythrocytic cycle is responsible for the clinical manifestations of malaria and can continue until the infection is eliminated by the host immune response or cleared by antimalarial drug treatment. Within red blood cells, individual merozoites will replicate their DNA 4 to 5 times within 48 hours and release 16 to 32 daughter merozoites back into the blood stream to infect other red blood cells. The mature merozoites are released from the hepatocytes and invade red blood cells. Human infection commences with the injection of sporozoite stages by the bite of an infectious mosquito asexual sporozoites then travel to the liver where they produce tens of thousands of merozoites after multiple rounds of DNA replication. Except for a brief diploid phase after mating events in the mosquito midgut, the parasite stages in both hosts are haploid. falciparum malaria parasite has a unique and complex life cycle involving multiple DNA replications both in the mosquito and in human hosts. Genome plasticity and genetic variation are significant challenges to vaccine development and contribute to the worldwide problem of drug resistance. Parasite resistance to multiple antimalarial drugs has also spread rapidly in recent years. The goal of developing an effective vaccine to control infection or disease has yet to be met. The human malaria parasite Plasmodium falciparum kills approximately one million people each year, mostly children in Africa. The lack of recombination activity in centromeric regions is consistent with the observations of reduced recombination near the centromeres of other organisms. GC-rich repetitive motifs identified in the hotspot sequences may play a role in the high recombination rate observed. ![]() 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. 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. falciparum centromeres are found in chromosome regions largely devoid of recombination activity. Similar to centromeres in other organisms, the sequences of P. Comparing genetic and physical maps, we obtained an overall recombination rate of 9.6 kb per centimorgan and identified 54 candidate recombination hotspots. We detected 638 recombination events and constructed a high-resolution genetic map. Here, we used a high-density tiling array to estimate the genetic recombination rate among 32 progeny of a P. A better understanding of these mechanisms may provide important information for studying parasite evolution, immune evasion and drug resistance. Genetic recombination and nucleotide substitution are the two major mechanisms that the parasite employs to generate genome diversity. The human malaria parasite Plasmodium falciparum survives pressures from the host immune system and antimalarial drugs by modifying its genome. ![]()
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