Chromosomal organisation of a gene family encoding rhoptry proteins in Plasmodium yoelii

Owen, Carolyn A.; Sinha, Katharine A.; Keen, Jane K.; Ogun, Solabomi A.; Holder, Anthony A.

doi:10.1016/s0166-6851(99)00015-8

Cited by 28 publications

(19 citation statements)

References 25 publications

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“…The chromosomal locations of Pfr2ha and -hb were determined using a P. falciparum linkage map (19; available at www.ncbi.nlm.nih.gov/Malaria/index.html). Pfr2ha and -hb are found in an internal location on the same contig on chromosome 13, in contrast to the subtelomeric location described for the Py235 genes in P. yoelii (12).…”

Section: Resultsmentioning

confidence: 62%

Identification of Proteins from Plasmodium falciparum That Are Homologous to Reticulocyte Binding Proteins in Plasmodium vivax

et al. 2001

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Plasmodium falciparum infections can be fatal, while P. vivax infections usually are not. A possible factor involved in the greater virulence of P. falciparum is that this parasite grows in red blood cells (RBCs) of all maturities whereas P. vivax is restricted to growth in reticulocytes, which represent only approximately 1% of total RBCs in the periphery. Two proteins, expressed at the apical end of the invasive merozoite stage from P. vivax, have been implicated in the targeting of reticulocytes for invasion by this parasite. A search of the P. falciparum genome databases has identified genes that are homologous to the P. vivax rbp-1 and -2 genes. Two of these genes are virtually identical over a large region of the 5 end but are highly divergent at the 3 end. They encode high-molecular-mass proteins of >300 kDa that are expressed in late schizonts and localized to the apical end of the merozoite. To test a potential role in merozoite invasion of RBCs, we analyzed the ability of these proteins to bind to mature RBCs and reticulocytes. No binding to mature RBCs or cell preparations enriched for reticulocytes was detected. We identified a parasite clone that lacks the gene for one of these proteins, showing that the gene is not required for normal in vitro growth. Antibodies to these proteins can inhibit merozoite invasion of RBCs.

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Section: Resultsmentioning

confidence: 62%

Identification of Proteins from Plasmodium falciparum That Are Homologous to Reticulocyte Binding Proteins in Plasmodium vivax

et al. 2001

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“…DNA was extracted from asynchronous parasites at 5 to 10% parasitemia as previously described (31). The sequences of internal primers RepF1, RepF2, and RepR, designed around the polymorphic region of stevor, have been published elsewhere (13).…”

Section: Methodsmentioning

confidence: 99%

Small Variant STEVOR Antigen Is Uniquely Located within Maurer's Clefts in Plasmodium falciparum -Infected Red Blood Cells

Kaviratne¹,

Khan²,

Jarra³

et al. 2002

Eukaryot Cell

118

140

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Malaria parasite antigens encoded by multigene families are important factors in virulence and in disease pathology. In Plasmodium falciparum, the virulence factor PfEMP-1 is encoded by the var multigene family and is exposed at the infected erythrocyte surface. PfEMP-1 is clonally variant, allowing the parasite to evade host immunity. The recently identified P. falciparum stevor multigene family and its products also have the potential to be involved in similar important aspects of host-parasite interactions. Here, we show tightly regulated stage-specific transcription of stevor occurring over just a few hours of the asexual parasite life cycle. Only a subset of stevor genes are transcribed in parasite populations maintained in cultures and in single micromanipulated parasites. Antibodies against STEVOR recognize proteins of the expected size (ϳ37 kDa) and localize STEVOR in Maurer's clefts, unique membranous structures located in the cytoplasm of infected erythrocytes. The fact that the timing of stevor expression and the location of STEVOR are clearly distinct from those of other parasite variant antigens suggests that this gene family may have a novel role in P. falciparum biology.To facilitate intraerythrocytic growth and survival, the asexual stage of malaria parasites makes extensive modifications to the parasitized host red blood cell (pRBC) (1). These modifications include the presentation of immunogenic parasite proteins at the surface of the pRBC, exposing the parasite to the effects of host immunity (14,25). Several of these surface proteins, for example, PfEMP-1 in Plasmodium falciparum and SICA antigen in P. knowelsi, induce antibody responses in the infected host which correlate with protection (11, 12). These molecules, encoded by multigene families, have also been shown to be clonally variant, allowing the parasite to evade host immunity. PfEMP-1, encoded by the var multigene family, facilitates the binding of pRBCs to a variety of host receptors on the endothelium, leading to the obstruction of blood vessels and contributing to the pathology and disease severity seen with P. falciparum. PfEMP-1 is thus considered a major virulence factor in P. falciparum infections in humans.Research on malaria multigene families has so far focused on var and rif in P. falciparum and py235 in P. yoelii. However, the Malaria Genome Project has now revealed additional families, including stevor in P. falciparum. Although relatively little is known about stevor, the possibility that its expression product, STEVOR, is involved in virulence, pathology, immunity, and immune evasion warrants more detailed investigation. First reported as 7h8, stevor was initially identified as an expressed sequence detected by a monoclonal antibody (29). There are about 30 to 40 copies of stevor per haploid genome, clustered within 50 kb of the telomeres on all chromosomes (13). Like rif, stevor has short first and longer (ϳ1-kb) second exons. The protein (STEVOR) has a predicted size of 30 to 40 kDa (13) and structurally may be simil...

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“…1). Chromosome mapping has shown that all py235 genes are located in the subtelomeric region of some but not all chromosomes (Owen et al, 1999). From the genome sequencing of other rodent parasites it has become apparent that orthologues of this family are present in P. berghei and P. chabaudi.…”

Section: Plasmodium Yoelii and Other Rodent Malaria Parasitesmentioning

confidence: 99%

Invasion of host cells by malaria parasites: a tale of two protein families

Iyer

Grüner

Rénia

et al. 2007

Molecular Microbiology

129

124

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SummaryMalaria parasites are obligate intracellular parasites whose invasive stages select and invade the unique host cell in which they can develop with exquisite specificity and efficacy. Most studies aimed at elucidating the molecules and the mechanisms implicated in the selection and invasion processes have been conducted on the merozoite, the stage that invades erythrocytes to perpetuate the pathological cycles of parasite multiplication in the blood. Bioinformatic analysis has helped identify the members of two parasite protein families, the reticulocyte-binding protein homologues (RBL) and erythrocyte binding like (EBL), in recently sequenced genomes of different Plasmodium species. In this article we review data from classical studies and gene disruption experiments that are helping to illuminate the role of these proteins in the selection-invasion processes. The manner in which subsets of proteins from each of the families act in concert suggests a model to explain the ability of the parasites to use alternate pathways of invasion. Future perspectives and implications are discussed.

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Chromosomal organisation of a gene family encoding rhoptry proteins in Plasmodium yoelii

Cited by 28 publications

References 25 publications

Identification of Proteins from Plasmodium falciparum That Are Homologous to Reticulocyte Binding Proteins in Plasmodium vivax

Identification of Proteins from Plasmodium falciparum That Are Homologous to Reticulocyte Binding Proteins in Plasmodium vivax

Small Variant STEVOR Antigen Is Uniquely Located within Maurer's Clefts in Plasmodium falciparum -Infected Red Blood Cells

Invasion of host cells by malaria parasites: a tale of two protein families

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