Stress induces the transcription of toxin-antitoxin systems but does not activate toxin
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ABSTRACT:
ORGANISM(S): Escherichia coli
PROVIDER: GSE141320 | GEO | 2020/06/11
REPOSITORIES: GEO
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Project description:The purpose of this study was to identify the RNA cleavage targets and specificities of 9 endoribonuclease toxins from toxin-antitoxin systems in E. coli MG1655.
2021-07-13 | GSE179607 | GEO
Project description:Rickettsia spp. can cause mild to severe human disease. These intracellular bacteria are associated with arthropods, nematodes and trematodes, and usually, are efficiently transmitted transovarially to the progeny of the invertebrate host. We recently demonstrated foreign gene acquisition by lateral gene transfer in Rickettsia genomes. The unexpected presence of laterally transferred toxin-antitoxin (TA) genetic elements (including vapBC) in several Rickettsia genomes has not been connected with the pathogenic process or the host-bacteria relationship. We suspect that vapBC are selfish genetic elements that addict eukaryotic hosts to Rickettsia. We identified a statistical link between the transovarial transmission of Rickettsia in invertebrate hosts and the presence of TA operons, specifically vapBC, in the Rickettsia genome. These TA are neighboring to type IV secretion genes. Tunel assays and whole-genome expression of infected cells showed that antibiotic eradication of TA-containing Rickettsia from the host in cell culture initiates a proapoptotic program. Rickettsia VapC toxins inhibit the growth of transformed Escherichia coli and Saccharomyces cerevisiae. Rickettsia toxin presents in vitro RNase activity. Annexin-V staining and time-lapse video showed that intracytoplasmic injections of VapC toxins in cells cause apoptosis. These data demonstrate that host cells may develop a dependence on Rickettsia spp. expressing the vapBC operon. This would constitute a new evolutionary M-bM-^@M-^\mafia strategyM-bM-^@M-^] of intracellular bacteria based on host addiction. Fresh cells from the human microvascular endothelial cell line (HMEC-1) [26] were infected with R. felis California-2 strain in the presence and absence of antibiotics, at a rate of 5 bacteria per eukaryotic cell. Then, we added or not antibiotics (chloramphenicol 50 M-BM-5g/ml or doxycycline to 40 M-BM-5g/ml) in both experimental (R.felis-infected) and control, mock-infected cells for 6 hours. The cells were harvested and RNA was extracted using the RNeasy Mini Kit (Qiagen). DNA contamination was removed using the Turbo DNA-free Kit (Ambion). RNA were labeled using the Quick Amp Labeling Kit One-color (Agilent) and hybridized onto a Whole Human Genome Microarray, 4x44K (Agilent) as recommended by the manufacturer. Arrays were scanned with DNA Microarray Scanner (Agilent), and data were extracted using Feature Extractor (Agilent).
2012-05-23 | E-GEOD-22072 | biostudies-arrayexpress
Project description:Type I toxin-antitoxin (TA) systems are widespread genetic modules in bacterial genomes. They express toxic peptides whose overexpression leads to growth arrest or cell death, whereas antitoxins regulate the expression of toxins, acting as labile antisense RNAs. The Staphylococcus aureus (S. aureus) genome contains and expresses several functional type I TA systems, but their biological functions remain unclear. Here we addressed and challenged experimentally, by proteomics, if a type I TA system, the SprF1/SprG1 pair, influences the overall gene expression in S. aureus. Deleted and complemented S. aureus strains were analyzed for their proteomes, both intracellular and extracellular, during growth. Comparison of intracellular proteomes between the strains points on SprF1 antitoxin as an agent downregulating protein expression. In the strain naturally expressing the SprG1 toxin, cytoplasmic proteins are excreted into the medium, but this is not due to unspecific cell leakages. Such toxin-driven release of the cytoplasmic proteins may modulate the host inflammatory response that, in turn, may amplify the S. aureus infection spread.
2021-07-05 | PXD023449 | Pride
Project description:Rickettsia spp. can cause mild to severe human disease. These intracellular bacteria are associated with arthropods, nematodes and trematodes, and usually, are efficiently transmitted transovarially to the progeny of the invertebrate host. We recently demonstrated foreign gene acquisition by lateral gene transfer in Rickettsia genomes. The unexpected presence of laterally transferred toxin-antitoxin (TA) genetic elements (including vapBC) in several Rickettsia genomes has not been connected with the pathogenic process or the host-bacteria relationship. We suspect that vapBC are selfish genetic elements that addict eukaryotic hosts to Rickettsia. We identified a statistical link between the transovarial transmission of Rickettsia in invertebrate hosts and the presence of TA operons, specifically vapBC, in the Rickettsia genome. These TA are neighboring to type IV secretion genes. Tunel assays and whole-genome expression of infected cells showed that antibiotic eradication of TA-containing Rickettsia from the host in cell culture initiates a proapoptotic program. Rickettsia VapC toxins inhibit the growth of transformed Escherichia coli and Saccharomyces cerevisiae. Rickettsia toxin presents in vitro RNase activity. Annexin-V staining and time-lapse video showed that intracytoplasmic injections of VapC toxins in cells cause apoptosis. These data demonstrate that host cells may develop a dependence on Rickettsia spp. expressing the vapBC operon. This would constitute a new evolutionary “mafia strategy” of intracellular bacteria based on host addiction.
2012-05-24 | GSE22072 | GEO
Project description:E.coli toxin-antitoxin systems
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Project description:Stress induces the transcription of toxin-antitoxin systems but does not activate toxin
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Project description:Bacterial type II toxin-antitoxin (TA) systems exhibit high specificity within each pair to ensure precise recognition of the toxin by its cognate antitoxin to inhibit toxicity of the free toxin. Despite high structural similarity among some TAs, crosstalk between noncognate TA pairs is rare. To determine how the E. coli RelB antitoxin suppresses its cognate RelE toxin, we engineered C-terminal truncations of RelB and tested their functional effects on toxin suppression in E. coli. We find that removal of the long Cterminal a3 and connecting loop 4 (L4) of RelB prevents RelE suppression. Quantitative binding assays of RelE and RelB variants support a reduced affinity upon removal of the RelB C-terminus. Disrupting these interactions between RelB and RelE also led to a significant decrease in transcriptional repression at the relO operator, underscoring the requirement for RelE binding to RelB for optimal repression at DNA repressor elements. Comparison to other structurally homologous TA systems, such as E. coli DinJ-YafQ, reveals key differences in the molecular mechanisms of both toxin suppression and DNA repressor activity highlighting the diversity in TA regulation and function.
2025-07-06 | PXD065338 | Pride
Project description:The role of six toxin-antitoxin (TA) systems on biofilm development was investigated (MazEF, RelBEF, ChpB, YefM-YoeB, DinJ-YafQ, and TomB-Hha). Although these TA systems were reported previously to not impact bacterial fitness, we found that biofilm formation is decreased by toxins and increased by anti-toxins, in part, through YjgK. Hence, one role of TA systems is to regulate biofilm formation. Experiment Overall Design: Strains: E. coli K-12 MG1655 and E. coli K-12 LVM100 delta 5 TA mutant Experiment Overall Design: Medium: LB Experiment Overall Design: Cells: biofilm cells on glass wool Experiment Overall Design: Time: 15 h Experiment Overall Design: Temperature: 37oC
2009-02-09 | E-GEOD-11932 | biostudies-arrayexpress
Project description:The role of six toxin-antitoxin (TA) systems on biofilm development was investigated (MazEF, RelBEF, ChpB, YefM-YoeB, DinJ-YafQ, and TomB-Hha). Although these TA systems were reported previously to not impact bacterial fitness, we found that biofilm formation is decreased by toxins and increased by anti-toxins, in part, through YjgK. Hence, one role of TA systems is to regulate biofilm formation. Experiment Overall Design: Strains: E. coli K-12 BW25113 wild-type and E. coli BW25113 yjgK deleted mutant Experiment Overall Design: Medium: LB Experiment Overall Design: Cells: biofilm cells on glass wool Experiment Overall Design: Time: 8 h Experiment Overall Design: Temperature: 37oC
2009-02-09 | E-GEOD-12701 | biostudies-arrayexpress
Project description:Conjugative plasmids, major vehicles for the spread of antibiotic resistance genes, often contain multiple toxin‒antitoxin (TA) systems. However, the physiological functions of TA systems remain obscure. By studying TA families commonly found on colistin-resistant IncI2 mcr-1-bearing plasmids, we discovered that the HicAB TA, acts as a crucial addiction module to increase horizontal plasmid‒plasmid competition.
2024-12-25 | GSE284789 | GEO