ArticleNature communications2024
Translation initiation factor eIF1.2 promotes Toxoplasma stage conversion by regulating levels of key differentiation factors.
Article in Nature communications, 2024. 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.
- PUF family RNA-binding proteins Puf1 and Puf2 promote transcript degradation in Toxoplasma gondii.The Journal of biological chemistry · 2026Article
- Structural basis for emetine inhibition of ribosome translocation inbioRxiv : the preprint server for biology · 2026Article
- Translational control of Toxoplasma gondii differentiation.Bioscience reports · 2026Review
- Modeling Toxoplasma gondii-gut early interactions using a human microphysiological system.PLoS neglected tropical diseases · 2025Article
- Novel Drug Targets for the Bradyzoite Form ofResearch and reports in tropical medicine · 2025Review
- Functional Characterization of Six Eukaryotic Translation Initiation Factors ofInternational journal of molecular sciences · 2024Article
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14 authors.
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Abstract
The parasite Toxoplasma gondii persists in its hosts by converting from replicating tachyzoites to latent bradyzoites housed in tissue cysts. The molecular mechanisms that mediate T. gondii differentiation remain poorly understood. Through a mutagenesis screen, we identified translation initiation factor eIF1.2 as a critical factor for T. gondii differentiation. A F97L mutation in eIF1.2 or the genetic ablation of eIF1.2 (∆eif1.2) markedly impeded bradyzoite cyst formation in vitro and in vivo. We demonstrated, at single-molecule level, that the eIF1.2 F97L mutation impacts the scanning process of the ribosome preinitiation complex on a model mRNA. RNA sequencing and ribosome profiling experiments unveiled that ∆eif1.2 parasites are defective in upregulating bradyzoite induction factors BFD1 and BFD2 during stress-induced differentiation. Forced expression of BFD1 or BFD2 significantly restored differentiation in ∆eif1.2 parasites. Together, our findings suggest that eIF1.2 functions by regulating the translation of key differentiation factors necessary to establish chronic toxoplasmosis.
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