T98G Cell Death Induced by Photothermal Treatment with Hollow Gold Nanoshell-Coupled Silica Microrods Prepared from Escherichia Coli

2019 ◽  
Vol 11 (9) ◽  
pp. 8831-8837 ◽  
Author(s):  
Soomin Han ◽  
Yoo-Jin Park ◽  
Eun-Jung Park ◽  
Younghun Kim
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
T98g Cell ◽  
Gold Nanoshell ◽  
Photothermal Treatment

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 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.

scholarly journals The Extracellular Death Factor: Physiological and Genetic Factors Influencing Its Production and Response in Escherichia coli

2008 ◽  
Vol 190 (9) ◽  
pp. 3169-3175 ◽  
Author(s):  
Ilana Kolodkin-Gal ◽  
Hanna Engelberg-Kulka
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Genetic Factors ◽  
Strain Differences ◽  
Lethal Effect ◽  
Mixed Population ◽  
Signal Molecule ◽  
Physiological Conditions ◽  
Dehydrogenase Gene ◽  
Glucose 6 Phosphate Dehydrogenase

ABSTRACT Gene pairs specific for a toxin and its antitoxin are called toxin-antitoxin modules and are found on the chromosomes of many bacteria. The most studied of these modules is Escherichia coli mazEF, in which mazF encodes a stable toxin, MazF, and mazE encodes a labile antitoxin, MazE, which prevents the lethal effect of MazF. In a previous report from this laboratory, it was shown that mazEF-mediated cell death is a population phenomenon requiring a quorum-sensing peptide called the extracellular death factor (EDF). EDF is the linear pentapeptide NNWNN (32). Here, we further confirm that EDF is a signal molecule in a mixed population. In addition, we characterize some physiological conditions and genes required for EDF production and response. Furthermore, stress response and the gene specifying MazEF, the Zwf (glucose-6-phosphate dehydrogenase) gene, and the protease ClpXP are critical in EDF production. Significant strain differences in EDF production and response explain variations in the induction of mazEF-mediated cell death.

scholarly journals A Single-Amino-Acid Substitution in Obg Activates a New Programmed Cell Death Pathway in Escherichia coli

mBio ◽  
2015 ◽  
Vol 6 (6) ◽  
Author(s):  
Liselot Dewachter ◽  
Natalie Verstraeten ◽  
Daniel Monteyne ◽  
Cyrielle Ines Kint ◽  
Wim Versées ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Surface ◽  
Single Amino Acid ◽  
Altruistic Behavior ◽  
Membrane Blebbing ◽  
Cell Death Pathway ◽  
Higher Eukaryotes ◽  
Multicellular Organisms

ABSTRACT Programmed cell death (PCD) is an important hallmark of multicellular organisms. Cells self-destruct through a regulated series of events for the benefit of the organism as a whole. The existence of PCD in bacteria has long been controversial due to the widely held belief that only multicellular organisms would profit from this kind of altruistic behavior at the cellular level. However, over the past decade, compelling experimental evidence has established the existence of such pathways in bacteria. Here, we report that expression of a mutant isoform of the essential GTPase ObgE causes rapid loss of viability in Escherichia coli. The physiological changes that occur upon expression of this mutant protein—including loss of membrane potential, chromosome condensation and fragmentation, exposure of phosphatidylserine on the cell surface, and membrane blebbing—point to a PCD mechanism. Importantly, key regulators and executioners of known bacterial PCD pathways were shown not to influence this cell death program. Collectively, our results suggest that the cell death pathway described in this work constitutes a new mode of bacterial PCD. IMPORTANCE Programmed cell death (PCD) is a well-known phenomenon in higher eukaryotes. In these organisms, PCD is essential for embryonic development—for example, the disappearance of the interdigital web—and also functions in tissue homeostasis and elimination of pathogen-invaded cells. The existence of PCD mechanisms in unicellular organisms like bacteria, on the other hand, has only recently begun to be recognized. We here demonstrate the existence of a bacterial PCD pathway that induces characteristics that are strikingly reminiscent of eukaryotic apoptosis, such as fragmentation of DNA, exposure of phosphatidylserine on the cell surface, and membrane blebbing. Our results can provide more insight into the mechanism and evolution of PCD pathways in higher eukaryotes. More importantly, especially in the light of the looming antibiotic crisis, they may point to a bacterial Achilles’ heel and can inspire innovative ways of combating bacterial infections, directed at the targeted activation of PCD pathways.

scholarly journals Cell Death in Escherichia coli dnaE(Ts) Mutants Incubated at a Nonpermissive Temperature Is Prevented by Mutation in the cydA Gene

2004 ◽  
Vol 186 (7) ◽  
pp. 2147-2155 ◽  
Author(s):  
Bernard Strauss ◽  
Kemba Kelly ◽  
Toros Dincman ◽  
Damian Ekiert ◽  
Theresa Biesieda ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Dna Synthesis ◽  
Dna Content ◽  
Electrophoretic Pattern ◽  
Luria Bertani ◽  
E Coli ◽  
Viable Cells ◽  
Rna And Protein Synthesis ◽  
Transformation Activity

ABSTRACT Cells of the Escherichia coli dnaE(Ts) dnaE74 and dnaE486 mutants die after 4 h of incubation at 40°C in Luria-Bertani medium. Cell death is preceded by elongation, is inhibited by chloramphenicol, tetracycline, or rifampin, and is dependent on cell density. Cells survive at 40°C when they are incubated at a high population density or at a low density in conditioned medium, but they die when the medium is supplemented with glucose and amino acids. Deletion of recA or sulA has no effect. We isolated suppressors which survived for long periods at 40°C but did not form colonies. The suppressors protected against hydroxyurea-induced killing. Sequence and complementation analysis indicated that suppression was due to mutation in the cydA gene. The DNA content of dnaE mutants increased about eightfold in 4 h at 40°C, as did the DNA content of the suppressed strains. The amount of plasmid pBR322 in a dnaE74 strain increased about fourfold, as measured on gels, and the electrophoretic pattern appeared to be normal even though the viability of the parent cells decreased 2 logs. Transformation activity also increased. 4′,6′-Diamidino-2-phenylindole staining demonstrated that there were nucleoids distributed throughout the dnaE filaments formed at 40°C, indicating that there was segregation of the newly formed DNA. We concluded that the DNA synthesized was physiologically competent, particularly since the number of viable cells of the suppressed strain increased during the first few hours of incubation. These observations support the view that E. coli senses the rate of DNA synthesis and inhibits septation when the rate of DNA synthesis falls below a critical level relative to the level of RNA and protein synthesis.

scholarly journals Dimethyl Sulfoxide Protects Escherichia coli from Rapid Antimicrobial-Mediated Killing

2016 ◽  
Vol 60 (8) ◽  
pp. 5054-5058 ◽  
Author(s):  
Hongfei Mi ◽  
Dai Wang ◽  
Yunxin Xue ◽  
Zhi Zhang ◽  
Jianjun Niu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Dimethyl Sulfoxide ◽  
Oxygen Species ◽  
Content Type ◽  
Antimicrobial Studies ◽  
Ros Accumulation ◽  
Short Time

ABSTRACTThe contribution of reactive oxygen species (ROS) to antimicrobial lethality was examined by treatingEscherichia coliwith dimethyl sulfoxide (DMSO), an antioxidant solvent frequently used in antimicrobial studies. DMSO inhibited killing by ampicillin, kanamycin, and two quinolones and had little effect on MICs. DMSO-mediated protection correlated with decreased ROS accumulation and provided evidence for ROS-mediated programmed cell death. These data support the contribution of ROS to antimicrobial lethality and suggest caution when using DMSO-dissolved antimicrobials for short-time killing assays.

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