ArticleMolecular microbiology2018
A Toxoplasma gondii locus required for the direct manipulation of host mitochondria has maintained multiple ancestral functions.
Article in Molecular microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Host-Parasite Interactions inInternational journal of molecular sciences · 2024Article
- Metabolic changes inmBio · 2024Article
- Susceptibility ofmBio · 2024Article
- Toxoplasma gondii mitochondrial association factor 1b interactome reveals novel binding partners including Ral GTPase accelerating protein α1.The Journal of biological chemistry · 2024Article
- Metabolic changes to host cells withbioRxiv : the preprint server for biology · 2023Article
- Host cell proteins modulated upon Toxoplasma infection identified using proteomic approaches: a molecular rationale.Parasitology research · 2022Review
- Manipulation of Host Cell Organelles by Intracellular Pathogens.International journal of molecular sciences · 2021Review
- Third-generation sequencing revises the molecular karyotype forGenome research · 2021Article
- Article
- Article
- Seizing control: How dense granule effector proteins enable Toxoplasma to take charge.Molecular microbiology · 2021Review
- Effector variation at tandem gene arrays in tissue-dwelling coccidia: who needs antigenic variation anyway?Current opinion in microbiology · 2018Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The Toxoplasma gondii locus mitochondrial association factor 1 (MAF1) encodes multiple paralogs, some of which mediate host mitochondrial association (HMA). Previous work showed that HMA was a trait that arose in T. gondii through neofunctionalization of an ancestral MAF1 ortholog. Structural analysis of HMA-competent and incompetent MAF1 paralogs (MAF1b and MAF1a, respectively) revealed that both paralogs harbor an ADP ribose binding macro-domain, with comparatively low (micromolar) affinity for ADP ribose. Replacing the 16 C-terminal residues of MAF1b with those of MAF1a abrogated HMA, and we also show that only three residues in the C-terminal helix are required for MAF1-mediated HMA. Importantly these same three residues are also required for the in vivo growth advantage conferred by MAF1b, providing a definitive link between in vivo proliferation and manipulation of host mitochondria. Co-immunoprecipitation assays reveal that the ability to interact with the mitochondrial MICOS complex is shared by HMA-competent and incompetent MAF1 paralogs and mutants. The weak ADPr coordination and ability to interact with the MICOS complex shared between divergent paralogs may represent modular ancestral functions for this tandemly expanded and diversified T. gondii locus.
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