ArticleScientific reports2016
Reactive oxygen species do not contribute to ObgE*-mediated programmed cell death.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
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- Targeting breast cancer stem cells in ER-positive breast cancer by repurposing the benzoporphyrin derivative verteporfin as a YAP/TAZ small molecule inhibitor.Molecular biology reports · 2025Article
- The role of the essential GTPase ObgE in regulating lipopolysaccharide synthesis in Escherichia coli.Nature communications · 2024Article
- Functional Characterization of Salmonella Typhimurium Encoded YciF, a Domain of Unknown Function (DUF892) Family Protein, and Its Role in Protection during Bile and Oxidative Stress.Journal of bacteriology · 2023Article
- Vibrio vulnificus induces the death of a major bacterial species in the mouse gut via cyclo-Phe-Pro.Microbiome · 2021Article
- Broad Spectrum Antibiotic Xanthocillin X Effectively KillsACS central science · 2021Article
- Redox signaling through zinc activates the radiation response in Deinococcus bacteria.Scientific reports · 2021Article
- GTP Binding is Necessary for the Activation of a Toxic Mutant Isoform of the Essential GTPase ObgE.International journal of molecular sciences · 2019Article
- A Combination of Linalool, Vitamin C, and Copper Synergistically Triggers Reactive Oxygen Species and DNA Damage and InhibitsApplied and environmental microbiology · 2019Article
- Arenicin-1-induced apoptosis-like response requires RecA activation and hydrogen peroxide against Escherichia coli.Current genetics · 2019Article
- A Mutant Isoform of ObgE Causes Cell Death by Interfering with Cell Division.Frontiers in microbiology · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed cell death (PCD) in bacteria is considered an important target for developing novel antimicrobials. Development of PCD-specific therapies requires a deeper understanding of what drives this process. We recently discovered a new mode of PCD in Escherichia coli that is triggered by expression of a mutant isoform of the essential ObgE protein, ObgE*. Our previous findings demonstrate that ObgE*-mediated cell death shares key characteristics with apoptosis in eukaryotic cells. It is well-known that reactive oxygen species (ROS) are formed during PCD in eukaryotes and play a pivotal role as signaling molecules in the progression of apoptosis. Therefore, we explored a possible role for ROS in bacterial killing by ObgE*. Using fluorescent probes and genetic reporters, we found that expression of ObgE* induces formation of ROS. Neutralizing ROS by chemical scavenging or by overproduction of ROS-neutralizing enzymes did not influence toxicity of ObgE*. Moreover, expression of ObgE* under anaerobic conditions proved to be as detrimental to bacterial viability as expression under aerobic conditions. In conclusion, ROS are byproducts of ObgE* expression that do not play a role in the execution or progression of ObgE*-mediated PCD. Targeted therapies should therefore look to exploit other aspects of ObgE*-mediated PCD.
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