ArticleMolecular microbiology2011
Functional analysis of epigenetic regulation of tandem RhopH1/clag genes reveals a role in Plasmodium falciparum growth.
Article in Molecular microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Distribution of Plasmodium falciparum apical membrane antigen-1 cluster one loop haplotypes and their association with malaria symptoms in Bandiagara, Mali.BMC infectious diseases · 2026Article
- An overview of the interconnectedness of the PEXEL and non-PEXEL mediated protein export iniScience · 2025Review
- Utilisation of an in vivo malaria model to provide functional proof for RhopH1/CLAG essentiality and conserved orthology with P. falciparum.Journal of biomedical science · 2025Article
- Guanidinium Chloride-Induced Haemolysis Assay to Measure New Permeation Pathway Functionality in Rodent MalariaBiomolecules · 2024Article
- Review
- Characterisation of complexes formed by parasite proteins exported into the host cell compartment of Plasmodium falciparum infected red blood cells.Cellular microbiology · 2021Article
- Non-ribosomal insights into ribosomal P2 protein in Plasmodium falciparum-infected erythrocytes.MicrobiologyOpen · 2021Article
- How Malaria Parasites Acquire Nutrients From Their Host.Frontiers in cell and developmental biology · 2021Review
- Complex nutrient channel phenotypes despite Mendelian inheritance in a Plasmodium falciparum genetic cross.PLoS pathogens · 2020Article
- Identification of Antimalarial Compounds That Require CLAG3 for Their Uptake byAntimicrobial agents and chemotherapy · 2019Article
- Expression and Localization Profiles of Rhoptry Proteins inFrontiers in cellular and infection microbiology · 2019Article
- Characterization of the accessible genome in the human malaria parasite Plasmodium falciparum.Nucleic acids research · 2018Article
- Comparative Heterochromatin Profiling Reveals Conserved and Unique Epigenome Signatures Linked to Adaptation and Development of Malaria Parasites.Cell host & microbe · 2018Article
- Malaria Epigenetics.Cold Spring Harbor perspectives in medicine · 2017Review
- Expression of the Plasmodium falciparum Clonally Variant clag3 Genes in Human Infections.The Journal of infectious diseases · 2017Article
- TheeLife · 2017Article
- Article
- Article
- Article
- Deciphering the principles that govern mutually exclusive expression of Plasmodium falciparum clag3 genes.Nucleic acids research · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The Plasmodium RhopH complex is a high molecular weight antigenic complex consisting of three subunits - RhopH1/clag, RhopH2 and RhopH3 - located in the rhoptry secretory organelles of the invasive merozoite. In Plasmodium falciparum RhopH1/clag is encoded by one of five clag genes. Two highly similar paralogous genes, clag 3.1 and clag 3.2, are mutually exclusively expressed. Here we show clonal switching from the clag 3.2 to the clag 3.1 paralogue in vitro. Chromatin immunoprecitation studies suggest that silencing of either clag 3 paralogue is associated with the enrichment of specific histone modifications associated with heterochromatin. We were able to disrupt the clag 3.2 gene, with a drug cassette inserted into the clag 3.2 locus being readily silenced in a position-dependent and sequence-independent manner. Activation of this drug cassette by drug selection results in parasites with the clag 3.1 locus silenced and lack full-length clag 3.1 or 3.2 transcripts. These clag 3-null parasites demonstrate a significant growth inhibition compared with wild-type parasites, providing the first genetic evidence for a role for these proteins in efficient parasite proliferation. Epigenetic regulation of these chromosomally proximal members of a multigene family provides a mechanism for both immune evasion and functional diversification.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.