ArticleMolecular microbiology2016
Developmental change in translation initiation alters the localization of a common microbial protein necessary for Toxoplasma chronic infection.
Article in Molecular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Immunomagnetic separation ofFrontiers in veterinary science · 2022Article
- The Toxoplasma gondii Cyst Wall Interactome.mBio · 2020Article
- Toxoplasma gondii: Bradyzoite Differentiation In Vitro and In Vivo.Methods in molecular biology (Clifton, N.J.) · 2020Article
- Proximity biotinylation reveals novel secreted dense granule proteins of Toxoplasma gondii bradyzoites.PloS one · 2020Article
- Article
- Observations on bradyzoite biology.Microbes and infectionReview
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The Toxoplasma gondii cyst stage is resistant to drug therapy. To identify potential targets for new therapeutics, we screened insertional mutants of T. gondii for a reduced ability to form cysts in the brains of mice. In one of these mutants, named 38C3, the mutagenesis plasmid inserted into the mRNA of a protein that is highly conserved in microbes but is not present in humans. The mutation in 38C3 causes reduced brain cyst production during chronic infection, but does not affect acute virulence, so the disrupted gene and protein are called T. gondii Brain Colonization Protein 1 (TgBCP1). TgBCP1 has three potential in frame start codons that produce 51, 33 or 25 kDa proteins. In rapidly replicating tachyzoites, translation initiates at the third methionine, producing the 25 kDa form that is conserved in many bacteria and protozoans. Brain cysts exclusively express the 51 kDa form of TgBCP1, which is secreted from the parasites and localizes to the cyst wall. Only expression of the long form of TgBCP1 restored cyst formation in the 38C3 mutant. TgBCP1 is essential for cyst formation and is the first example of a developmental regulation in translation initiation site preference for a T. gondii protein.
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