ArticleCommunications biology2025
Deletion of ESX-3 and ESX-4 secretion systems in Mycobacterium abscessus results in highly impaired pathogenicity.
Article in Communications biology, 2025. 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.
- Morphological plasticity facilitates lung adaptation and dynamic immune remodeling in Mycobacterium abscessus infection.iScience · 2026Article
- Acidic pH Restricts Non-Tuberculous Mycobacteria Replication.Molecular microbiology · 2026Article
- Sigma factor M induces an ESX-4-focused regulon inFrontiers in tuberculosis · 2026Article
- Protein Architecture and Composition in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- EccC3 is essential for pathogenesis of roughMicrobiology spectrum · 2025Article
- Animal models of Mycobacterium abscessus pulmonary infection phenotypes: What are we modeling?PLoS pathogens · 2025Article
- Article
- Insights on the Pathogenesis ofJournal of clinical medicine · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Type VII secretion systems participate in protein export, virulence, conjugation, and metabolic regulation. Five subtypes (ESX-1 to ESX-5) exist, each with specific roles and well-characterized secretion profiles in various mycobacterial species. Mycobacterium abscessus, encodes only ESX-3 and ESX-4. Here, single and double M. abscessus mutants lacking the main ATPases EccC3 and EccC4 were used to define ESX-3 and ESX-4 contributions to substrate secretion and virulence. Our results demonstrate that EsxG/H secretion depends entirely on ESX-3, whereas both ESX-3 and ESX-4 secrete EsxU/T. Furthermore, two newly identified PE/PPE substrates (MAB_0046/MAB_0047) require ESX-3 for secretion. Functional complementation restored secretion and revealed subpolar localization of these systems. Macrophage infections showed that ESX-3 and ESX-4 contribute to bacterial internalization, phagosomal escape, and intracellular survival. In mice, infections with eccC3- and/or eccC4-deletion mutants resulted in complete survival and reduced bacterial loads in the lungs. These findings demonstrate that both ESX systems drive M. abscessus pathogenicity.
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