ArticleMolecular and biochemical parasitology2007
A Toxoplasma gondii mutant defective in responding to calcium fluxes shows reduced in vivo pathogenicity.
Article in Molecular and biochemical parasitology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Live-attenuated ME49Δcdpk3 strain of Toxoplasma gondii protects against acute and chronic toxoplasmosis.NPJ vaccines · 2022Article
- AmBio · 2019Article
- A Window toPathogens (Basel, Switzerland) · 2018Review
- Transcriptional repression by ApiAP2 factors is central to chronic toxoplasmosis.PLoS pathogens · 2018Article
- A novel dense granule protein, GRA41, regulates timing of egress and calcium sensitivity in Toxoplasma gondii.Cellular microbiology · 2017Article
- Analysis of Noncanonical Calcium-Dependent Protein Kinases in Toxoplasma gondii by Targeted Gene Deletion Using CRISPR/Cas9.Infection and immunity · 2016Article
- Guanabenz repurposed as an antiparasitic with activity against acute and latent toxoplasmosis.Antimicrobial agents and chemotherapy · 2015Article
- The calcium-dependent protein kinase 3 of toxoplasma influences basal calcium levels and functions beyond egress as revealed by quantitative phosphoproteome analysis.PLoS pathogens · 2014Article
- Bradyzoite pseudokinase 1 is crucial for efficient oral infectivity of the Toxoplasma gondii tissue cyst.Eukaryotic cell · 2013Article
- Role of gap junctions and hemichannels in parasitic infections.BioMed research international · 2013Review
- Prison break: pathogens' strategies to egress from host cells.Microbiology and molecular biology reviews : MMBR · 2012Review
- A forward genetic screen reveals that calcium-dependent protein kinase 3 regulates egress in Toxoplasma.PLoS pathogens · 2012Article
- A Toxoplasma gondii protein with homology to intracellular type Na⁺/H⁺ exchangers is important for osmoregulation and invasion.Experimental cell research · 2011Article
- Calcium storage and function in apicomplexan parasites.Essays in biochemistry · 2011Review
- Exit from host cells by the pathogenic parasite Toxoplasma gondii does not require motility.Eukaryotic cell · 2008Article
- Article
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4 authors.
Funding
Abstract
Toxoplasma gondii is an important opportunistic pathogen in immunocompromised individuals. Successful propagation in an infected host by this obligate intracellular parasite depends on its ability to enter and exit host cells. Egress from the cell can be artificially induced by causing fluxes of calcium within the parasite with the use of calcium ionophores. While this ionophore-induced egress (IIE) has been characterized in detail, it is not known whether it mimics a normal physiological process of the parasite. This is underscored by the fact that mutants in IIE do not exhibit strong defects in any of the normal growth characteristics of the parasite in tissue culture. We have isolated and characterized a T. gondii mutant that along with a delay in IIE exhibits a severe defect in establishing a successful infection in vivo. In tissue culture this mutant displays normal ability to invade, divide within cells and convert into the latent encysted bradyzoite form. Nevertheless, mice infected with this mutant are less likely to die and carry less brain cysts than those infected with wild type parasites. Thus, our results suggest that normal response to calcium fluxes plays an important role during in vivo development of T. gondii.
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