ArticleJournal of bacteriology2011
Membrane proteases and aminoglycoside antibiotic resistance.
Article in Journal of bacteriology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
What it found
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Who cites it
58 citing papers in PubMed, 102 citations in OpenAlex.
- Selective Reprogramming of Ribosome Assembly and Translational Control during Bacterial Growth Phase Transitions.ACS omega · 2026Article
- Structural plasticity of the membrane-bound protein degradation assembly supports bacterial adaptation to stress.Cell reports · 2026Article
- Exploring the Diversity and Function of the SPFH-Domain Containing Proteins in Pseudomonas aeruginosa.Environmental microbiology reports · 2026Article
- Activation of the envelope stress-responsive two-component system AmgRS compensates for depletion of the essential lipoprotein signal peptidase LspA inCurrent research in microbial sciences · 2026Article
- Selective silencing of antibiotic-tethered ribosomes as a resistance mechanism against aminoglycosides.Nature communications · 2025Article
- Structural Plasticity of the Membrane-Bound Protein Degradation Assembly Supports Bacterial Adaptation to Stress.bioRxiv : the preprint server for biology · 2025Article
- Phase-Specific Antibiotic Resistance Mechanisms in anbioRxiv : the preprint server for biology · 2025Article
- Antibiotic-induced stress responses in Gram-negative bacteria and their role in antibiotic resistance.The Journal of antimicrobial chemotherapy · 2025Review
- An asymmetric nautilus-like HflK/C assembly controls FtsH proteolysis of membrane proteins.The EMBO journal · 2025Article
- Protein profile of the Escherichia coli strain, BW25113, exposed to two novel iron-halide compounds: Fe(Hampy)2Cl4 and Fe(Hampy)2Br4.Access microbiology · 2025Article
- Malonate is relevant to the lung environment and induces genome-wide stress responses in Pseudomonas aeruginosa.Research square · 2024Article
- An asymmetric nautilus-like HflK/C assembly controls FtsH proteolysis of membrane proteins.bioRxiv : the preprint server for biology · 2024Article
- Lipase and Protease Production Ability of Multi-drug Resistant Bacteria Worsens the Outcomes of Wound Infections.Current pharmaceutical design · 2024Article
- Aminoglycoside uptake, stress, and potentiation in Gram-negative bacteria: new therapies with old molecules.Microbiology and molecular biology reviews : MMBR · 2023Review
- Escherichia coli SPFH Membrane Microdomain Proteins HflKC Contribute to Aminoglycoside and Oxidative Stress Tolerance.Microbiology spectrum · 2023Article
- Gene-Gene Interactions Reduce Aminoglycoside Susceptibility ofAntibiotics (Basel, Switzerland) · 2023Article
- Targeting the Holy Triangle of Quorum Sensing, Biofilm Formation, and Antibiotic Resistance in Pathogenic Bacteria.Microorganisms · 2022Review
- The Wsp system ofProceedings of the National Academy of Sciences of the United States of America · 2022Article
- A comparative whole-genome approach identifies bacterial traits for marine microbial interactions.Communications biology · 2022Article
- Conserved Tandem Arginines for PbgA/YejM Allow Salmonella Typhimurium To Regulate LpxC and Control Lipopolysaccharide Biogenesis during Infection.Infection and immunity · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
We present genetic studies that help define the functional network underlying intrinsic aminoglycoside resistance in Pseudomonas aeruginosa. Our analysis shows that proteolysis, particularly that controlled by the membrane protease FtsH, is a major determinant of resistance. First, we examined the consequences of inactivating genes controlled by AmgRS, a two-component regulator required for intrinsic tobramycin resistance. Three of the gene products account for resistance: a modulator of FtsH protease (YccA), a membrane protease (HtpX), and a membrane protein of unknown function (PA5528). Second, we screened mutations inactivating 66 predicted proteases and related functions. Insertions inactivating two FtsH protease accessory factors (HflK and HflC) and a cytoplasmic protease (HslUV) increased tobramycin sensitivity. Finally, we generated an ftsH deletion mutation. The mutation dramatically increased aminoglycoside sensitivity. Many of the functions whose inactivation increased sensitivity appeared to act independently, since multiple mutations led to additive or synergistic effects. Up to 500-fold increases in tobramycin sensitivity were observed. Most of the mutations also were highly pleiotropic, increasing sensitivity to a membrane protein hybrid, several classes of antibiotics, alkaline pH, NaCl, and other compounds. We propose that the network of proteases provides robust protection from aminoglycosides and other substances through the elimination of membrane-disruptive mistranslation products.
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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.