ArticlePLoS pathogens2013
Francisella tularensis harvests nutrients derived via ATG5-independent autophagy to support intracellular growth.
Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
86 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Protection of macrophages from intracellular pathogens by miR-182-5p mimic-a gene expression meta-analysis approach.The FEBS journal · 2018Pooled it
- Modulatory Role of ATG5 Protein in Immune Modulation During Experimental Tularemia.Microorganisms · 2026Article
- Infectious bacteria as biological warfare agents: mechanisms, epidemiological threats, and defense strategies.Frontiers in bioengineering and biotechnology · 2026Review
- The battle between bacterial infection and autophagy in aquatic animals.Frontiers in immunology · 2025Review
- A novel method of Francisella infection of epithelial cells using HeLa cells expressing fc gamma receptor.BMC infectious diseases · 2024Article
- Endothelial Mechanistic Target of Rapamycin Activation with Different Strains ofMicroorganisms · 2024Article
- Breaking the cellular defense: the role of autophagy evasion inFrontiers in cellular and infection microbiology · 2024Article
- Diverse roles of low-molecular weight thiol GSH inCurrent research in microbial sciences · 2024Article
- Pathogenicity and virulence ofVirulence · 2023Review
- Francisella tularensis Exploits AMPK Activation to Harvest Host-Derived Nutrients Liberated from Host Lipolysis.Infection and immunity · 2022Article
- Alternative autophagy: mechanisms and roles in different diseases.Cell communication and signaling : CCS · 2022Review
- Recruitment of LC3 byFrontiers in cellular and infection microbiology · 2022Article
- Interaction Between Autophagy andFrontiers in cellular and infection microbiology · 2022Review
- Molecular mechanisms and clinical implications of multiple forms of mitophagy in the heart.Cardiovascular research · 2021Review
- Moments in autophagy and disease: Past and present.Molecular aspects of medicine · 2021Review
- Autophagy in major human diseases.The EMBO journal · 2021Review
- Autophagy-A Story of Bacteria Interfering with the Host Cell Degradation Machinery.Pathogens (Basel, Switzerland) · 2021Review
- Atg5-Deficient Mice Infected withMicroorganisms · 2020Article
- SON DNA-binding protein mediates macrophage autophagy and responses to intracellular infection.FEBS letters · 2020Article
- The cell biology of inflammation: From common traits to remarkable immunological adaptations.The Journal of cell biology · 2020Review
26 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
6 authors at 1 institution in 1 country.
Funding
Abstract
Francisella tularensis is a highly virulent intracellular pathogen that invades and replicates within numerous host cell types including macrophages, hepatocytes and pneumocytes. By 24 hours post invasion, F. tularensis replicates up to 1000-fold in the cytoplasm of infected cells. To achieve such rapid intracellular proliferation, F. tularensis must scavenge large quantities of essential carbon and energy sources from the host cell while evading anti-microbial immune responses. We found that macroautophagy, a eukaryotic cell process that primarily degrades host cell proteins and organelles as well as intracellular pathogens, was induced in F. tularensis infected cells. F. tularensis not only survived macroautophagy, but optimal intracellular bacterial growth was found to require macroautophagy. Intracellular growth upon macroautophagy inhibition was rescued by supplying excess nonessential amino acids or pyruvate, demonstrating that autophagy derived nutrients provide carbon and energy sources that support F. tularensis proliferation. Furthermore, F. tularensis did not require canonical, ATG5-dependent autophagy pathway induction but instead induced an ATG5-independent autophagy pathway. ATG5-independent autophagy induction caused the degradation of cellular constituents resulting in the release of nutrients that the bacteria harvested to support bacterial replication. Canonical macroautophagy limits the growth of several different bacterial species. However, our data demonstrate that ATG5-independent macroautophagy may be beneficial to some cytoplasmic bacteria by supplying nutrients to support bacterial growth.
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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.