ArticlePLoS pathogens2022
The ESX-4 substrates, EsxU and EsxT, modulate Mycobacterium abscessus fitness.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Sec and Tat Mediated Secretion Safeguards Mycobacterium tuberculosis Membrane Homeostasis.Molecular & cellular proteomics : MCP · 2026Article
- Whole-genome recombination and dynamic accessory genomes drive the phenotypic diversity of Mycobacterium abscessus subspecies.Annals of clinical microbiology and antimicrobials · 2025Article
- Review
- Deletion of ESX-3 and ESX-4 secretion systems in Mycobacterium abscessus results in highly impaired pathogenicity.Communications biology · 2025Article
- Article
- Evolution and emergence of Mycobacterium tuberculosis.FEMS microbiology reviews · 2024Review
- The small non-coding RNA B11 regulates multiple facets of Mycobacterium abscessus virulence.PLoS pathogens · 2023Article
- The cell envelope of Mycobacterium abscessus and its role in pathogenesis.PLoS pathogens · 2023Review
- Role of the Mycobacterium tuberculosis ESX-4 Secretion System in Heme Iron Utilization and Pore Formation by PPE Proteins.mSphere · 2023Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ESX type VII secretion systems are complex secretion machineries spanning across the mycobacterial membrane and play an important role in pathogenicity, nutrient uptake and conjugation. We previously reported the role of ESX-4 in modulating Mycobacterium abscessus intracellular survival. The loss of EccB4 was associated with limited secretion of two effector proteins belonging to the WXG-100 family, EsxU and EsxT, and encoded by the esx-4 locus. This prompted us to investigate the function of M. abscessus EsxU and EsxT in vitro and in vivo. Herein, we show that EsxU and EsxT are substrates of ESX-4 and form a stable 1:1 heterodimer that permeabilizes artificial membranes. While expression of esxU and esxT was up-regulated in M. abscessus-infected macrophages, their absence in an esxUT deletion mutant prevented phagosomal membrane disruption while maintaining M. abscessus in an unacidified phagosome. Unexpectedly, the esxUT deletion was associated with a hyper-virulent phenotype, characterised by increased bacterial loads and mortality in mouse and zebrafish infection models. Collectively, these results demonstrate that the presence of EsxU and EsxT dampens survival and persistence of M. abscessus during infection.
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Registered trials
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