ArticlePLoS pathogens2011
Autophagy protein Atg3 is essential for maintaining mitochondrial integrity and for normal intracellular development of Toxoplasma gondii tachyzoites.
Article in PLoS pathogens, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 3 of them syntheses that pooled it.
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Who cites it
77 citing papers in PubMed, 3 syntheses or guidelines pooled it, 134 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
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- Mitophagy-mediated immune evasion: Shared strategies of pathogens.Redox biology · 2026Review
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- Tepsin and AP4 mediate transport from the trans-Golgi to the plant-like vacuole in toxoplasma.The Journal of cell biology · 2025Article
- HIV-1 Tat favors the multiplication of Mycobacterium tuberculosis and Toxoplasma by inhibiting clathrin-mediated endocytosis and autophagy.PLoS pathogens · 2025Article
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- Gold(I) ion and the phosphine ligand are necessary for the anti-Microbiology spectrum · 2024Article
- Regulation of Atg8 membrane deconjugation by cysteine proteases in the malaria parasite Plasmodium berghei.Cellular and molecular life sciences : CMLS · 2023Article
- An essential role for an Fe-S cluster protein in the cytochrome c oxidase complex of Toxoplasma parasites.PLoS pathogens · 2023Article
- Apicoplast biogenesis mediated by ATG8 requires the ATG12-ATG5-ATG16L and SNAP29 complexes inAutophagy · 2023Article
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- Two small-molecule inhibitors ofFrontiers in cellular and infection microbiology · 2023Article
- Autophagy in protists and their hosts: When, how and why?Autophagy reports · 2023Article
- A VPS15-like kinase regulates apicoplast biogenesis and autophagy by promoting PI3P generation in Toxoplasma gondii.PLoS pathogens · 2022Article
- The Toxoplasma plant-like vacuolar compartment (PLVAC).The Journal of eukaryotic microbiology · 2022Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Autophagy is a cellular process that is highly conserved among eukaryotes and permits the degradation of cellular material. Autophagy is involved in multiple survival-promoting processes. It not only facilitates the maintenance of cell homeostasis by degrading long-lived proteins and damaged organelles, but it also plays a role in cell differentiation and cell development. Equally important is its function for survival in stress-related conditions such as recycling of proteins and organelles during nutrient starvation. Protozoan parasites have complex life cycles and face dramatically changing environmental conditions; whether autophagy represents a critical coping mechanism throughout these changes remains poorly documented. To investigate this in Toxoplasma gondii, we have used TgAtg8 as an autophagosome marker and showed that autophagy and the associated cellular machinery are present and functional in the parasite. In extracellular T. gondii tachyzoites, autophagosomes were induced in response to amino acid starvation, but they could also be observed in culture during the normal intracellular development of the parasites. Moreover, we generated a conditional T. gondii mutant lacking the orthologue of Atg3, a key autophagy protein. TgAtg3-depleted parasites were unable to regulate the conjugation of TgAtg8 to the autophagosomal membrane. The mutant parasites also exhibited a pronounced fragmentation of their mitochondrion and a drastic growth phenotype. Overall, our results show that TgAtg3-dependent autophagy might be regulating mitochondrial homeostasis during cell division and is essential for the normal development of T. gondii tachyzoites.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.