ArticleThe Journal of biological chemistry2015
Pseudomonas aeruginosa ExoT Induces Mitochondrial Apoptosis in Target Host Cells in a Manner That Depends on Its GTPase-activating Protein (GAP) Domain Activity.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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47 citing papers in PubMed, 73 citations in OpenAlex.
- Furin inhibition protects against acute lung injury in a mouse model of Pseudomonas aeruginosa infection.American journal of respiratory cell and molecular biology · 2026Article
- Pseudomonas aeruginosa Impairs Mitochondrial Function During Infection of Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2026Article
- Prevalence and genotypic distribution of virulence factor genes and antibiotic susceptibility profiles in clinicalMicrobiology spectrum · 2026Article
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- Blepharitis driven by microbiome dysbiosis andFrontiers in medicine · 2026Review
- Interplay between T3SS effectors, ExoY activation, and cGMP signaling in Pseudomonas aeruginosa infection.Nature communications · 2025Article
- Carbon source-driven downregulation of the sRNA AmiL enhancesVirulence · 2025Article
- Advances inMicroorganisms · 2025Review
- Phage-encoded protein PavP modulates Pseudomonas aeruginosa virulence by dual inhibition of growth and pathogenic traits.Biology direct · 2025Article
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- High prevalence of carbapenem-resistantFrontiers in microbiology · 2025Article
- Carbapenem-resistantFrontiers in pharmacology · 2025Article
- Targeting PANoptosis in Bacterial-Induced Inflammatory Diseases: Mechanisms and Therapeutic Interventions.Journal of inflammation research · 2025Review
- PemB, a type III secretion effector inHeliyon · 2024Article
- Mitochondrial Dysfunction in Bacterial Infections.Pathogens (Basel, Switzerland) · 2023Review
- Anti-Microorganisms · 2023Review
- Synthetic biology-inspired cell engineering in diagnosis, treatment, and drug development.Signal transduction and targeted therapy · 2023Review
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- Airway Epithelial Cell Junctions as Targets for Pathogens and Antimicrobial Therapy.Pharmaceutics · 2022Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Pseudomonas aeruginosa is the most common cause of hospital-acquired pneumonia and a killer of immunocompromised patients. We and others have demonstrated that the type III secretion system (T3SS) effector protein ExoT plays a pivotal role in facilitating P. aeruginosa pathogenesis. ExoT possesses an N-terminal GTPase-activating protein (GAP) domain and a C-terminal ADP-ribosyltransferase (ADPRT) domain. Because it targets multiple non-overlapping cellular targets, ExoT performs several distinct virulence functions for P. aeruginosa, including induction of apoptosis in a variety of target host cells. Both the ADPRT and the GAP domain activities contribute to ExoT-induced apoptosis. The ADPRT domain of ExoT induces atypical anoikis by transforming an innocuous cellular protein, Crk, into a cytotoxin, which interferes with integrin survival signaling. However, the mechanism underlying the GAP-induced apoptosis remains unknown. In this study, we demonstrate that the GAP domain activity is both necessary and sufficient to induce mitochondrial (intrinsic) apoptosis. We show that intoxication with GAP domain results in: (i) JNK1/2 activation; (ii) substantial increases in the mitochondrial levels of activated pro-apoptotic proteins Bax and Bid, and to a lesser extent Bim; (iii) loss of mitochondrial membrane potential and cytochrome c release; and (iv) activation of initiator caspase-9 and executioner caspase-3. Further, GAP-induced apoptosis is partially mediated by JNK1/2, but it is completely dependent on caspase-9 activity. Together, the ADPRT and the GAP domains make ExoT into a highly versatile and potent cytotoxin, capable of inducing multiple forms of apoptosis in target host cells.
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