ArticleParasites & vectors2022
Depletion of Toxoplasma adenine nucleotide translocator leads to defects in mitochondrial morphology.
Article in Parasites & vectors, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Unconventional model organisms bend our view on mitochondrial cristae.Journal of cell science · 2026Review
- ZFT is the major iron and zinc transporter ineLife · 2026Article
- Transporters, an important but poorly studied area of Toxoplasma gondii.Parasites & vectors · 2026Review
- Article
- Metabolic crosstalk between the mitochondrion and the nucleus is essential for Toxoplasma gondii infection.Communications biology · 2025Article
- ATM1, an essential conserved transporter in Apicomplexa, bridges mitochondrial and cytosolic [Fe-S] biogenesis.PLoS pathogens · 2024Article
- Iron Stress Affects the Growth and Differentiation ofInternational journal of molecular sciences · 2024Article
- TgMORN2, a MORN Family Protein Involved in the Regulation of Endoplasmic Reticulum Stress inInternational journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAdenine nucleotide translocase (ANT) is a protein that catalyzes the exchange of ADP/ATP across the inner mitochondrial membrane. Beyond this, ANT is closely associated with cell death pathways and mitochondrial dysfunction. It is a potential therapeutic target for many diseases. The function of the ANT in Toxoplasma gondii is poorly understood.
methodsThe CRISPR/CAS9 gene editing tool was used to identify and study the function of the ANT protein in T. gondii. We constructed T. gondii ANT transgenic parasite lines, including endogenous tag strain, knockout strain and gene complement strain, to clarify the function and location of TgANT. Mitochondrial morphology was observed by immunofluorescence and transmission electron microscopy.
resultsToxoplasma gondii was found to encode an ANT protein, which was designated TgANT. TgANT localized to the inner mitochondrial membrane. The proliferation of the Δant strain was significantly reduced. More important, depletion of TgANT resulted in significant changes in the morphology and ultrastructure of mitochondria, abnormal apicoplast division and abnormal cytoskeletal daughter budding. In addition, the pathogenicity of the Δant strain to mice was significantly reduced.
conclusionsAltogether, we identified and characterized the ANT protein of T. gondii. Depletion of TgANT inhibited parasite growth and impaired apicoplast and mitochondrial biogenesis, as well as abnormal parasite division, suggesting TgANT is important for parasite growth.
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