ArticleInfection and immunity2008
Evidence for pore formation in host cell membranes by ESX-1-secreted ESAT-6 and its role in Mycobacterium marinum escape from the vacuole.
Article in Infection and immunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers.
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Who cites it
164 citing papers in PubMed, 290 citations in OpenAlex.
- Review
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- Targeting Autophagy as a Strategy for Developing New Host-Directed Therapeutics Against Nontuberculous Mycobacteria.Pathogens (Basel, Switzerland) · 2025Review
- Mitochondrial DNA signals driving immune responses: Why, How, Where?Cell communication and signaling : CCS · 2025Review
- Insights into Autophagy in Microbiome Therapeutic Approaches for Drug-Resistant Tuberculosis.Cells · 2025Review
- Real-time visualization reveals Mycobacterium tuberculosis ESAT-6 disrupts phagosome-like compartment via fibril-mediated vesiculation.Cell reports · 2025Article
- Single-cell analysis revealsScience advances · 2025Article
- Type VII secretion system gene mutations driving global mycobacterium tuberculosis transmission revealed by whole genomic sequence.Frontiers in cellular and infection microbiology · 2025Article
- EsxA, a type VII secretion system-dependent effector, reveals a novel function in the sporulation of Bacillus cereus ATCC14579.BMC microbiology · 2024Article
- Exploring host-pathogen interactions in the Dictyostelium discoideum-Mycobacterium marinum infection model of tuberculosis.Disease models & mechanisms · 2024Review
- ESAT-6 undergoes self-association at phagosomal pH and an ESAT-6-specific nanobody restrictseLife · 2024Article
- The antagonistic transcription factors, EspM and EspN, regulate the ESX-1 secretion system inmBio · 2024Article
- ESAT-6 undergoes self-association at phagosomal pH and an ESAT-6 specific nanobody restricts M. tuberculosis growth in macrophages.bioRxiv : the preprint server for biology · 2024Article
- Temporal genome-wide fitness analysis ofmSystems · 2024Article
- Article
- The role of ESAT-6 in tuberculosis immunopathology.Frontiers in immunology · 2024Review
- Phylogenetic analysis of prospective M. bovis antigens with the aim of developing candidate vaccines for bovine tuberculosis.Journal, genetic engineering & biotechnology · 2023Article
- Mitochondrial reactive oxygen species: double agents in Mycobacterium tuberculosis infection.Current opinion in immunology · 2023Review
- Emerging Extracellular Molecular Targets for Innovative Pharmacological Approaches to Resistant Mtb Infection.Biomolecules · 2023Review
- Autophagy restricts Mycobacterium tuberculosis during acute infection in mice.Nature microbiology · 2023Article
104 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The ESX-1 secretion system plays a critical role in the virulence of M. tuberculosis and M. marinum, but the precise molecular and cellular mechanisms are not clearly defined. Virulent M. marinum is able to escape from the Mycobacterium-containing vacuole (MCV) into the host cell cytosol, polymerize actin, and spread from cell to cell. In this study, we have examined nine M. marinum ESX-1 mutants and the wild type by using fluorescence and electron microscopy detecting MCV membranes and actin polymerization. We conclude that ESX-1 plays an essential role in M. marinum escape from the MCV. We also show that the ESX-1 mutants acquire the ability to polymerize actin after being artificially delivered into the macrophage cytosol by hypotonic shock treatment, indicating that ESX-1 is not directly involved in initiation of actin polymerization. We provide evidence that M. marinum induces membrane pores approximately 4.5 nm in diameter, and this activity correlates with ESAT-6 secretion. Importantly, purified ESAT-6, but not the other ESX-1-secreted proteins, is able to cause dose-dependent pore formation in host cell membranes. These results suggest that ESAT-6 secreted by M. marinum ESX-1 could play a direct role in producing pores in MCV membranes, facilitating M. marinum escape from the vacuole and cell-to-cell spread. Our study provides new insight into the mechanism by which ESX-1 secretion and ESAT-6 enhance the virulence of mycobacterial infection.
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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.