ArticleMolecular microbiology2013
A molecular switch in the efficiency of translation reinitiation controls expression of var2csa, a gene implicated in pregnancy-associated malaria.
Article in Molecular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Mechanistic insights into coordinated var transcriptional switching in malaria parasites.The EMBO journal · 2026Article
- Evolutionary Trajectory ofBiomedicines · 2025Review
- Variable surface antigen expression, virulence, and persistent infection byMicrobiology and molecular biology reviews : MMBR · 2025Review
- Hemozoin: a waste product after heme detoxification?Parasites & vectors · 2025Article
- Transcription and Copy Number Variation of Plasmodium falciparum var2csa among Nonpregnant Malaria Patients in Thailand.The American journal of tropical medicine and hygiene · 2025Article
- PfEMP1 and var genes - Still of key importance in Plasmodium falciparum malaria pathogenesis and immunity.Advances in parasitology · 2024Review
- What exactly does the PfK13 C580Y mutation in Plasmodium falciparum influence?Parasites & vectors · 2023Article
- The human malaria parasiteProceedings of the National Academy of Sciences of the United States of America · 2023Article
- A coordinated transcriptional switching network mediates antigenic variation of human malaria parasites.eLife · 2022Article
- Functional characterization of 5' UTR cis-acting sequence elements that modulate translational efficiency in Plasmodium falciparum and humans.Malaria journal · 2022Article
- The role of upstream open reading frames in translation regulation in the apicomplexan parasitesParasitology · 2021Review
- Evolution of transcriptional control of antigenic variation and virulence in human and ape malaria parasites.BMC ecology and evolution · 2021Article
- Article
- Protein-RNA interactions important for Plasmodium transmission.PLoS pathogens · 2019Review
- Global genetic diversity of var2csa in Plasmodium falciparum with implications for malaria in pregnancy and vaccine development.Scientific reports · 2018Article
- An upstream open reading frame (uORF) signals for cellular localization of the virulence factor implicated in pregnancy associated malaria.Nucleic acids research · 2018Article
- Plasmodium falciparum Recrudescence Two Years after Treatment of an Uncomplicated Infection without Return to an Area Where Malaria Is Endemic.Antimicrobial agents and chemotherapy · 2018Article
- Translational Control in the Latency of Apicomplexan Parasites.Trends in parasitology · 2017Review
- Red blood cells release microparticles containing human argonaute 2 and miRNAs to target genes of Plasmodium falciparum.Emerging microbes & infections · 2017Article
- Article
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2 authors at 1 institution in 1 country.
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Abstract
Plasmodium falciparum malaria parasites export the protein PfEMP1 to the surface of infected erythrocytes, enabling them to adhere to receptors in the microvasculature and thereby avoid clearance by the spleen. The gene var2csa encodes the form of PfEMP1 that binds specifically within the placenta, causing pregnancy-associated malaria, and appears to not be expressed in the absence of a placenta. We previously described an upstream open reading frame (uORF) that is responsible for repression of translation of the downstream ORF (dORF) that encodes VAR2CSA, thus keeping the gene silent when parasites infect non-pregnant individuals. To elucidate the molecular mechanism by which this repression is overcome during pregnancy, we stably transformed parasites with reporter gene constructs designed to detect switches in the efficiency of dORF translation. We found that proper regulation of switching relies on two separate components, (i) active translation of the uORF and (ii) sequence-specific characteristics of the surrounding transcript, which together control the ability of the ribosome complex to reinitiate a second round of translation and thus express VAR2CSA. These results provide the first details of a molecular switch that allows parasites take advantage of the unique niche provided by the placenta.
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