ArticlePLoS pathogens2017
Calmodulin-like proteins localized to the conoid regulate motility and cell invasion by Toxoplasma gondii.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 131 citations in OpenAlex.
- A conserved GTPase complex gates exocytosis for defence and parasitism across alveolates.Nature microbiology · 2026Article
- Article
- Clustering of host N-glycans by the microneme MIC1/4/6 complex licenses Toxoplasma rhoptry discharge.The EMBO journal · 2026Article
- Organization of Myosin H in the Apical Complex ofbioRxiv : the preprint server for biology · 2026Article
- Assessing theBio-protocol · 2026Article
- Atomic models of the Toxoplasma cell invasion machinery.Nature structural & molecular biology · 2026Article
- A Spinster-like Transporter at the Inner Membrane Complex is critical for Toxoplasma gondii cytokinesis, motility and invasion.PLoS pathogens · 2026Article
- An ER-resident lipid scramblase is crucial for biogenesis and function of apicomplexan parasite secretory organelles.Nature communications · 2025Article
- Evolutionarily convergent mechanism of formin regulation coordinates actin polymerization in apicomplexan parasites.Science advances · 2025Article
- Article
- Function and interactions of a protein bridge between the inner membrane complex and subpellicular microtubules inMolecular biology of the cell · 2025Article
- The Major Facilitator Superfamily Transporter HAP12 Is Critical inInternational journal of molecular sciences · 2025Article
- Molecular mechanisms of surface antigen suppression by ApiAP2 and its implications for vaccine development.Veterinary research · 2025Article
- Expanding the CRISPR/Cas toolkit: applications in proteomics and theranostics.Frontiers in bioengineering and biotechnology · 2025Review
- Establishment of an ELISA for detecting oocyst-derivedFrontiers in veterinary science · 2025Article
- Functional dissection of prenyltransferases reveals roles in endocytosis and secretory vacuolar sorting in type 2-ME49 strain ofVirulence · 2024Article
- Establishment of the auxin inducible degron system for Babesia duncani: a conditional knockdown tool to study precise protein regulation in Babesia spp.Parasites & vectors · 2024Article
- Orthologs ofMicrobiology spectrum · 2024Article
- Calcium-binding protein TgpCaBP regulates calcium storage of the zoonotic parasiteMicrobiology spectrum · 2024Article
- TBC9, an essential TBC-domain protein, regulates early vesicular transport and IMC formation in Toxoplasma gondii.Communications biology · 2024Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Toxoplasma gondii contains an expanded number of calmodulin (CaM)-like proteins whose functions are poorly understood. Using a combination of CRISPR/Cas9-mediated gene editing and a plant-like auxin-induced degron (AID) system, we examined the roles of three apically localized CaMs. CaM1 and CaM2 were individually dispensable, but loss of both resulted in a synthetic lethal phenotype. CaM3 was refractory to deletion, suggesting it is essential. Consistent with this prediction auxin-induced degradation of CaM3 blocked growth. Phenotypic analysis revealed that all three CaMs contribute to parasite motility, invasion, and egress from host cells, and that they act downstream of microneme and rhoptry secretion. Super-resolution microscopy localized all three CaMs to the conoid where they overlap with myosin H (MyoH), a motor protein that is required for invasion. Biotinylation using BirA fusions with the CaMs labeled a number of apical proteins including MyoH and its light chain MLC7, suggesting they may interact. Consistent with this hypothesis, disruption of MyoH led to degradation of CaM3, or redistribution of CaM1 and CaM2. Collectively, our findings suggest these CaMs may interact with MyoH to control motility and cell invasion.
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.