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 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 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 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 “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.

Thermal and Starvation Stress Response of Escherichia coli O157:H7 Isolates Selected from Agricultural Environments

2016 ◽  
Vol 79 (10) ◽  
pp. 1673-1679 ◽  
Author(s):  
ACHYUT ADHIKARI ◽  
ANDY BARY ◽  
CRAIG COGGER ◽  
CALEB JAMES ◽  
GÜLHAN ÜNLÜ ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Heat Stress ◽  
Stress Response ◽  
Weibull Model ◽  
Stress Conditions ◽  
Inactivation Kinetics ◽  
Escherichia Coli O157 ◽  
Starvation Stress ◽  
E Coli ◽  
Response To Stress

ABSTRACT Pathogens exposed to agricultural production environments are subject to multiple stresses that may alter their survival under subsequent stress conditions. The objective of this study was to examine heat and starvation stress response of Escherichia coli O157:H7 strains isolated from agricultural matrices. Seven E. coli O157:H7 isolates from different agricultural matrices—soil, compost, irrigation water, and sheep manure—were selected, and two ATCC strains were used as controls. The E. coli O157:H7 isolates were exposed to heat stress (56°C in 0.1% peptone water for up to 1 h) and starvation (in phosphate-buffered saline at 37°C for 15 days), and their survival was examined. GInaFiT freeware tool was used to perform regression analyses of the surviving populations. The Weibull model was identified as the most appropriate model for response of the isolates to heat stress, whereas the biphasic survival curves during starvation were fitted using the double Weibull model, indicating the adaptation to starvation or a resistant subpopulation. The inactivation time during heating to achieve the first decimal reduction time (δ) calculated with the Weibull parameters was the highest (45 min) for a compost isolate (Comp60A) and the lowest (28 min) for ATCC strain 43895. Two of the nine isolates (ATCC 43895 and a manure isolate) had β < 1, indicating that surviving populations adapted to heat stress, and six strains demonstrated downward concavity (β > 1), indicating decreasing heat resistance over time. The ATCC strains displayed the longest δ2 (>1,250 h) in response to starvation stress, compared with from 328 to 812 h for the environmental strains. The considerable variation in inactivation kinetics of E. coli O157:H7 highlights the importance of evaluating response to stress conditions among individual strains of a specific pathogen. Environmental isolates did not exhibit more robust response to stress conditions in this study compared with ATCC strains.

Programmed Cell Death in Plants: Insights Into developmental and Stress-Induced Cell Death

2021 ◽  
Vol 22 ◽  
Author(s):  
Heba T. Ebeed ◽  
Ahmed A. El-helely
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Plant Development ◽  
Molecular Basis ◽  
Stress Conditions ◽  
Similar Form ◽  
Cellular Homeostasis ◽  
Endogenous Factors ◽  
Selective Elimination

: Programmed cell death (PCD) is a fundamental genetically controlled process in most organisms. PCD is responsible for the selective elimination of damaged or unwanted cells and organs to maintain cellular homeostasis during the organ’s development under normal conditions as well as during defense or adaptation to stressful conditions. PCD pathways have been extensively studied in animals. In plants, studies focusing on understanding the pathways of PCD have advanced significantly. However, the knowledge about the molecular basis of PCD is still very limited. Some PCD pathways that have been discovered in animals are not present in plants or found with a similar form. PCD in plants is developmentally controlled (by endogenous factors) to function in organ development and differentiations as well as environmentally induced (by exogenous stimuli) to help the plant in surviving under stress conditions. Here, we present a review of the role of PCD in plant development and explore different examples of stress-induced PCD as well as highlight the main differences between the plant and animal PCD.

scholarly journals Flight muscles degenerate by programmed cell death after migration in the wheat aphid, Sitobion avenae

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Honglin Feng ◽  
Xiao Guo ◽  
Hongyan Sun ◽  
Shuai Zhang ◽  
Jinghui Xi ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Molecular Mechanism ◽  
Differentially Expressed Genes ◽  
Flight Muscle ◽  
Sitobion Avenae ◽  
Differentially Expressed ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Muscle Degeneration ◽  
Flight Muscles

Abstract Objective Previous studies showed that flight muscles degenerate after migration in some aphid species; however, the underlying molecular mechanism remains virtually unknown. In this study, using the wheat aphid, Sitobion avenae, we aim to investigate aphid flight muscle degeneration and the underlying molecular mechanism. Results Sitobion avenae started to differentiate winged or wingless morphs at the second instar, the winged aphids were fully determined at the third instar, and their wings were fully developed at the fourth instar. After migration, the aphid flight muscles degenerated via programmed cell death, which is evidenced by a Terminal deoxynucleotidyl transferase dUTP-biotin nick-end labeling assay. Then, we identified a list of differentially expressed genes before and after tethered flights using differential-display reverse transcription-PCR. One of the differentially expressed genes, ubiquitin-ribosomal S27a, was confirmed using qPCR. Ubiquitin-ribosomal S27a is drastically up regulated following the aphids’ migration and before the flight muscle degeneration. Our data suggested that aphid flight muscles degenerate after migration. During flight muscle degeneration, endogenous proteins may be degraded to reallocate energy for reproduction.

scholarly journals Induction of Escherichia coli Chromosomal mazEF by Stressful Conditions Causes an Irreversible Loss of Viability

2006 ◽  
Vol 188 (9) ◽  
pp. 3420-3423 ◽  
Author(s):  
Ilana Kolodkin-Gal ◽  
Hanna Engelberg-Kulka
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Basic Characteristic ◽  
Irreversible Loss ◽  
Previous Conclusion ◽  
E Coli ◽  
Programmed Death

ABSTRACT mazEF is a stress-induced toxin-antitoxin module located on the chromosomes of many bacteria. Here we induced Escherichia coli chromosomal mazEF by various stressful conditions. We found an irreversible loss of viability, which is the basic characteristic of cell death. These results further support our previous conclusion that E. coli mazEF mediation of cell death is not a passive process, but an active and genetically “programmed” death response.

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