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The unique structure of the apicoplast genome of the rodent malaria parasite Plasmodium chabaudi chabaudi.

ABSTRACT: The apicoplast, a non-photosynthetic plastid of apicomplexan species, has an extremely reduced but highly conserved genome. Here, the apicoplast genome of the rodent malaria parasite Plasmodium chabaudi chabaudi (Pcc) isolate CB was characterized. Although the set of genes in the genome is identical, the copy number of some tRNA genes differs between Pcc and other Plasmodium species because the Pcc DNA has only one rRNA/tRNA gene cluster, which is normally duplicated in other species. The location of the duplicated trnR(ACG) and trnM implies that one of the duplicated clusters in the ancestral molecule has been lost due to an intramolecular recombination event. The Pcc DNA occurs in two isoforms with an internal inversion between them. The presence of a unique variant in the duplicated trnT gene suggests that the two isoforms are interconvertible. This is the first report of the complete nucleotide sequence of a Plasmodium apicoplast DNA.

SUBMITTER: Sato S

PROVIDER: S-EPMC3627918 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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The unique structure of the apicoplast genome of the rodent malaria parasite Plasmodium chabaudi chabaudi.

Sato Shigeharu S Sato Shigeharu S Sesay Abdul K AK Holder Anthony A AA

PloS one 20130416 4

The apicoplast, a non-photosynthetic plastid of apicomplexan species, has an extremely reduced but highly conserved genome. Here, the apicoplast genome of the rodent malaria parasite Plasmodium chabaudi chabaudi (Pcc) isolate CB was characterized. Although the set of genes in the genome is identical, the copy number of some tRNA genes differs between Pcc and other Plasmodium species because the Pcc DNA has only one rRNA/tRNA gene cluster, which is normally duplicated in other species. The locati ...[more]

PMID: 23613931

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Project description:BackgroundThe ability of malaria (Plasmodium) parasites to adjust investment into sexual transmission stages versus asexually replicating stages is well known, but plasticity in other traits underpinning the replication rate of asexual stages in the blood has received less attention. Such traits include burst size (the number of merozoites produced per schizont), the duration of the asexual cycle, and invasion preference for different ages of red blood cell (RBC).MethodsHere, plasticity [environment (E) effects] and genetic variation [genotype (G) effects] in traits relating to asexual replication rate are examined for 4 genotypes of the rodent malaria parasite Plasmodium chabaudi. An experiment tested whether asexual dynamics differ between parasites infecting control versus anaemic hosts, and whether variation in replication rate can be explained by differences in burst size, asexual cycle, and invasion rates.ResultsThe within-host environment affected each trait to different extents but generally had similar impacts across genotypes. The dynamics of asexual densities exhibited a genotype by environment effect (G×E), in which one of the genotypes increased replication rate more than the others in anaemic hosts. Burst size and cycle duration varied between the genotypes (G), while burst size increased and cycle duration became longer in anaemic hosts (E). Variation in invasion rates of differently aged RBCs was not explained by environmental or genetic effects. Plasticity in burst size and genotype are the only traits making significant contributions to the increase in asexual densities observed in anaemic hosts, together explaining 46.4% of the variation in replication rate.ConclusionsThat host anaemia induces several species of malaria parasites to alter conversion rate is well documented. Here, previously unknown plasticity in other traits underpinning asexual replication is revealed. These findings contribute to mounting evidence that malaria parasites deploy a suite of sophisticated strategies to maximize fitness by coping with, or exploiting the opportunities provided by, the variable within-host conditions experienced during infections. That genetic variation and genotype by environment interactions also shape these traits highlights their evolutionary potential. Asexual replication rate is a major determinant of virulence and so, understanding the evolution of virulence requires knowledge of the ecological (within-host environment) and genetic drivers of variation among parasites.

Dataset Information

The unique structure of the apicoplast genome of the rodent malaria parasite Plasmodium chabaudi chabaudi.

Publications

The unique structure of the apicoplast genome of the rodent malaria parasite Plasmodium chabaudi chabaudi.

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