scholarly journals Postsegregational Killing Mediated by the P1 Phage “Addiction Module” phd-doc Requires the Escherichia coli Programmed Cell Death SystemmazEF

2001 ◽  
Vol 183 (6) ◽  
pp. 2046-2050 ◽  
Author(s):  
Ronen Hazan ◽  
Boaz Sat ◽  
Myriam Reches ◽  
Hanna Engelberg-Kulka
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Protein Synthesis ◽  
Programmed Cell Death ◽  
Killing Effect ◽  
E Coli ◽  
Lethal Action ◽  
Free Cells ◽  
Postsegregational Killing

ABSTRACT “Addiction modules” consist of two genes; the product of the second is long lived and toxic, while the product of the first is short lived and antagonizes the lethal action of the toxin. The extrachromosomal addiction module phd-doc, located on the P1 prophage, is responsible for the postsegregational killing effect (death of plasmid-free cells). The Escherichia colichromosomal addiction module analogue, mazEF, is responsible for the induction of programmed cell death. Here we show that the postsegregational killing mediated by the P1phd-doc module depends on the presence of the E. coli mazEF system. In addition, we demonstrate that under conditions of postsegregational killing, mediated byphd-doc, protein synthesis of E. coli is inhibited. Based on our findings, we suggest the existence of a coupling between the phd-doc and mazEFsystems.

scholarly journals MazF-Mediated Cell Death in Escherichia coli: a Point of No Return

2004 ◽  
Vol 186 (24) ◽  
pp. 8295-8300 ◽  
Author(s):  
Shahar Amitai ◽  
Yussuf Yassin ◽  
Hanna Engelberg-Kulka
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Inhibitory Effect ◽  
Luria Bertani ◽  
E Coli ◽  
Ectopic Overexpression ◽  
Point Of No Return ◽  
The Rich ◽  
Overexpression System

ABSTRACT mazEF is a stress-induced toxin-antitoxin module, located on the chromosome of Escherichia coli, that we have previously described to be responsible for programmed cell death in E. coli. mazF specifies a stable toxin, and mazE specifies a labile antitoxin. Recently, it was reported that inhibition of translation and cell growth by ectopic overexpression of the toxin MazF can be reversed by the action of the antitoxin MazE ectopically overexpressed at a later time. Based on these results, it was suggested that rather than inducing cell death, mazF induces a state of reversible bacteriostasis (K. Pederson, S. K. Christensen, and K. Gerdes, Mol. Microbiol. 45:501-510, 2002). Using a similar ectopic overexpression system, we show here that overexpression of MazE could reverse MazF lethality only over a short window of time. The size of that window depended on the nature of the medium in which MazF was overexpressed. Thus, we found “a point of no return,” which occurred sooner in minimal M9 medium than it did in the rich Luria-Bertani medium. We also describe a state in which the effect of MazF on translation could be separated from its effect on cell death: MazE overproduction could completely reverse the inhibitory effect of MazF on translation, while not affecting the bacteriocidic effect of MazF at all. Our results reported here support our view that the mazEF module mediates cell death and is part of a programmed cell death network.

scholarly journals The Action of Bacteriophage Ω8 on Two Strains of Escherichia coli 08

Microbiology ◽  
2000 ◽  
Vol 81 (1) ◽  
pp. 131-144 ◽  
Author(s):  
Barbara Wallenfels ◽  
K. Jann
Keyword(s):  
Escherichia Coli ◽  
Protein Synthesis ◽  
Phage Particle ◽  
Cytoplasmic Membrane ◽  
Cellular Respiration ◽  
Bacterial Strains ◽  
Viral Dna ◽  
Killing Effect ◽  
E Coli ◽  
Phage Propagation

Bacteriophage Ω8 is propagated in Escherichia coli E56b (08: K27-:H-), a non-capsulated strain. Another non-capsulated strain, E. coli 2398 (08:K?-:H-), is killed by bacteriophage Ω8 without phage propagation. This strain was formerly believed to be E. coli 093:K?-:H-, cross-reacting with strain E56b. We have established chemical and serological identity of the 08-specific lipopolysaccharides of the two strains. The 08-specific lipopolysaccharides of both strains inhibited the infection of Escherichia coli E56b with bacteriophage Ω8 equally well. The adsorption rate constants of Ω8 were identical for the two strains of E. coli 08. Evidence was obtained with 32P-labelled bacteriophage Ω8 for penetration of viral DNA into both bacterial strains. In host strain E56b, phage particle synthesis occurred normally. In strain 2398 the viral DNA was not degraded but its expression was blocked. The killing effect of Ω8 on E. coli strain 2398 is supposed to be due to damage of the cytoplasmic membrane, which could not be reversed under the influence of viral information. This was indicated by a blockage of cellular respiration, β-galactoside transport and RNA as well as protein synthesis.

scholarly journals Programmed Cell Death in Escherichia coli: Some Antibiotics Can Trigger mazEFLethality

2001 ◽  
Vol 183 (6) ◽  
pp. 2041-2045 ◽  
Author(s):  
Boaz Sat ◽  
Ronen Hazan ◽  
Tova Fisher ◽  
Hanita Khaner ◽  
Gad Glaser ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Bacterial Chromosome ◽  
E Coli ◽  
Bacterial Cultures ◽  
Gene Pairs ◽  
System A ◽  
Extrachromosomal Elements

ABSTRACT The discovery of toxin-antitoxin gene pairs (also called addiction modules) on extrachromosomal elements of Escherichia coli, and particularly the discovery of homologous modules on the bacterial chromosome, suggest that a potential for programmed cell death may be inherent in bacterial cultures. We have reported on the E. coli mazEF system, a regulatable addiction module located on the bacterial chromosome. MazF is a stable toxin and MazE is a labile antitoxin. Here we show that cell death mediated by the E. coli mazEF module can be triggered by several antibiotics (rifampicin, chloramphenicol, and spectinomycin) that are general inhibitors of transcription and/or translation. These antibiotics inhibit the continuous expression of the labile antitoxin MazE, and as a result, the stable toxin MazF causes cell death. Our results have implications for the possible mode(s) of action of this group of antibiotics.

scholarly journals Properties of a Revertant of Escherichia coli Viable in the Presence of Spermidine Accumulation: Increase in l-Glycerol 3-Phosphate

2001 ◽  
Vol 183 (15) ◽  
pp. 4493-4498 ◽  
Author(s):  
V. Samuel Raj ◽  
Hideyuki Tomitori ◽  
Madoka Yoshida ◽  
Auayporn Apirakaramwong ◽  
Keiko Kashiwagi ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Protein Synthesis ◽  
Glycerol Kinase ◽  
High Concentration ◽  
Gene Encoding ◽  
E Coli ◽  
Inhibition Of Protein Synthesis ◽  
High Concentrations ◽  
Ribosome Modulation Factor

ABSTRACT Escherichia coli CAG2242 cells are deficient in thespeG gene encoding spermidine acetyltransferase. When these cells were cultured in the presence of 0.5 to 4 mM spermidine, their viability was greatly decreased through the inhibition of protein synthesis by overaccumulation of spermidine. When the cells were cultured with a high concentration of spermidine (4 mM), a revertant strain was obtained. We found that a 55-kDa protein, glycerol kinase, was overexpressed in the revertant and that synthesis of a ribosome modulation factor and the RNA polymerase ς38 subunit, factors important for cell viability, was increased in the revertant. Levels of l-glycerol 3-phosphate also increased in the revertant. Transformation of glpFK, which encodes a glycerol diffusion facilitator (glpF) and glycerol kinase (glpK), to E. coli CAG2242 partially prevented the cell death caused by accumulation of spermidine. It was also found that l-glycerol 3-phosphate inhibited spermidine binding to ribosomes and attenuated the inhibition of protein synthesis caused by high concentrations of spermidine. These results indicate that l-glycerol 3-phosphate reduces the binding of excess amounts of spermidine to ribosomes so that protein synthesis is recovered.

scholarly journals The Escherichia coli mazEF Suicide Module Mediates Thymineless Death

2003 ◽  
Vol 185 (6) ◽  
pp. 1803-1807 ◽  
Author(s):  
Boaz Sat ◽  
Myriam Reches ◽  
Hanna Engelberg-Kulka
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanism ◽  
Stress Conditions ◽  
E Coli ◽  
System A ◽  
Thymine Starvation ◽  
Thymineless Death

ABSTRACT In 1954, Cohen and Barner discovered that a thymine auxotrophic (thyA) mutant of Escherichia coli undergoes cell death in response to thymine starvation. This phenomenon, called thymineless death (TLD), has also been found in many other organisms, including prokaryotes and eukaryotes. Though TLD has been studied intensively, its molecular mechanism has not yet been explained. Previously we reported on the E. coli mazEF system, a regulatable chromosomal suicide module that can be triggered by various stress conditions. MazF is a stable toxin, and MazE is an unstable antitoxin. Here, we show that cell death that is mediated by the mazEF module can also be activated by thymine starvation. We found that TLD depends on E. coli mazEF and that under thymine starvation, the activity of the mazEF promoter P2 is significantly reduced. Our results, which describe thymine starvation as a trigger for a built-in death program, have implications for programmed cell death in both prokaryotes and eukaryotes.

scholarly journals “mazEFmediated programmed cell death in Escherichia coli”: is it?

2016 ◽  
Author(s):  
Bhaskar Chandra Mohan Ramisetty ◽  
Swati Raj ◽  
Dimpy Ghosh
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Stress Tolerance ◽  
Type Ii ◽  
Overlapping Genes ◽  
Wild Type ◽  
E Coli ◽  
Typical Type ◽  
Metabolic Fitness

AbstractToxin-antitoxins systems (TAS) are prokaryotic operons containing two small overlapping genes which encode two components referred to as Toxin and Antitoxin. Involvement of TAS in bacterial programmed cell death (PCD) is highly controversial. MazEF, a typical type II TAS, is particularly implicated in mediating PCD inEscherichia coli. Hence, we compared the metabolic fitness and stress tolerance ofE. colistrains (MC4100 and itsmazEF- derivative) which were extensively used by proponents ofmazEF- mediated PCD. We found that both the strains are deficient inrelAgene and that theΔmazEFstrain has lower fitness and stress tolerance compared to wild type MC4100. Furthermore, these strains are likely not isogenic. We could not reproducemazEFmediated PCD which emphasizes the need for skeptic approach to the PCD hypothesis.

scholarly journals Escherichia coli K12 Upregulates Programmed Cell Death Ligand 1 (PD-L1) Expression in Gamma Interferon-Sensitized Intestinal Epithelial Cells via the NF-κB Pathway

2020 ◽  
Vol 89 (1) ◽  
pp. e00618-20 ◽  
Author(s):  
Seul A. Lee ◽  
Yiming Wang ◽  
Fang Liu ◽  
Stephen M. Riordan ◽  
Lu Liu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Bacterial Species ◽  
Intestinal Epithelial ◽  
Content Type ◽  
E Coli ◽  
Inflammatory Conditions ◽  
Ifn Γ ◽  
Ht 29

ABSTRACTProgrammed cell death ligand-1 (PD-L1) is an immune checkpoint protein which is used by tumor cells for immune evasion. PD-L1 is upregulated in inflamed intestinal tissues. The intestinal tract is colonized by millions of bacteria, most of which are commensal bacterial species. We hypothesized that under inflammatory conditions, some commensal bacterial species contribute to increased PD-L1 expression in intestinal epithelium and examined this hypothesis. Human intestinal epithelial HT-29 cells with and without interferon (IFN)-γ sensitization were incubated with six strains of four enteric bacterial species. The mRNA and protein levels of PD-L1 in HT-29 cells were examined using quantitative real-time PCR and flow cytometry, respectively. The levels of interleukin (IL)-1β, IL-18, IL-6, IL-8, and tumor necrosis factor (TNF)-α secreted by HT-29 cells were measured using enzyme-linked immunosorbent assay. Apoptosis of HT-29 cells was measured using a caspase 3/7 assay. We found that Escherichia coli K12 significantly upregulated both PD-L1 mRNA and protein in IFN-γ-sensitized HT-29 cells. E. coli K12 induced the production of IL-8 in HT-29 cells, however, IL-8 did not affect HT-29 PD-L1 expression. Inhibition of the nuclear factor-kappa B pathway significantly reduced E. coli K12-induced PD-L1 expression in HT-29 cells. The other two E. coli strains and two enteric bacterial species did not significantly affect PD-L1 expression in HT-29 cells. Enterococcus faecalis significantly inhibited PD-L1 expression due to induction of cell death. Data from this study suggest that some gut bacterial species have the potential to affect immune function under inflammatory conditions via upregulating epithelial PD-L1 expression.

scholarly journals Lethal Action of Quinolones against a Temperature-Sensitive dnaB Replication Mutant of Escherichia coli

2006 ◽  
Vol 50 (1) ◽  
pp. 362-364 ◽  
Author(s):  
Xilin Zhao ◽  
Muhammad Malik ◽  
Nymph Chan ◽  
Alex Drlica-Wagner ◽  
Jian-Ying Wang ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Protein Synthesis ◽  
Dna Replication ◽  
Nalidixic Acid ◽  
Temperature Sensitive ◽  
Wild Type ◽  
Lethal Action ◽  
Inhibition Of Protein Synthesis

ABSTRACT Inhibition of DNA replication in an Escherichia coli dnaB-22 mutant failed to block quinolone-mediated lethality. Inhibition of protein synthesis by chloramphenicol inhibited nalidixic acid lethality and, to a lesser extent, ciprofloxacin lethality in both dnaB-22 and wild-type cells. Thus, major features of quinolone-mediated lethality do not depend on ongoing replication.

scholarly journals Nerve growth factor withdrawal-induced cell death in neuronal PC12 cells resembles that in sympathetic neurons.

1992 ◽  
Vol 119 (6) ◽  
pp. 1669-1680 ◽  
Author(s):  
P W Mesner ◽  
T R Winters ◽  
S H Green
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Nerve Growth Factor ◽  
Growth Factor ◽  
Programmed Cell Death ◽  
Pc12 Cells ◽  
Sympathetic Neurons ◽  
Nerve Growth ◽  
Neuronal Pc12 Cells ◽  
New Protein

Previous studies have shown that in neuronal cells the developmental phenomenon of programmed cell death is an active process, requiring synthesis of both RNA and protein. This presumably reflects a requirement for novel gene products to effect cell death. It is shown here that the death of nerve growth factor-deprived neuronal PC12 cells occurs at the same rate as that of rat sympathetic neurons and, like rat sympathetic neurons, involves new transcription and translation. In nerve growth factor-deprived neuronal PC12 cells, a decline in metabolic activity, assessed by uptake of [3H]2-deoxyglucose, precedes the decline in cell number, assessed by counts of trypan blue-excluding cells. Both declines are prevented by actinomycin D and anisomycin. In contrast, the death of nonneuronal (chromaffin-like) PC12 cells is not inhibited by transcription or translation inhibitors and thus does not require new protein synthesis. DNA fragmentation by internucleosomal cleavage does not appear to be a consistent or significant aspect of cell death in sympathetic neurons, neuronal PC12 cells, or nonneuronal PC12 cells, notwithstanding that the putative nuclease inhibitor aurintricarboxylic acid protects sympathetic neurons, as well as neuronal and nonneuronal PC12 cells, from death induced by trophic factor removal. Both phenotypic classes of PC12 cells respond to aurintricarboxylic acid with similar dose-response characteristics. Our results indicate that programmed cell death in neuronal PC12 cells, but not in nonneuronal PC12 cells, resembles programmed cell death in sympathetic neurons in significant mechanistic aspects: time course, role of new protein synthesis, and lack of a significant degree of DNA fragmentation.

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