scholarly journals Potassium deprivation is sufficient  to induce a cell death program in Saccharomyces cerevisiae

2010 ◽  
pp. no-no ◽  
Author(s):  
Diana Beatríz Lauff ◽  
Guillermo E. Santa-María
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Cell Death Program ◽  
A Cell ◽  
Potassium Deprivation

scholarly journals Hypoxic neuronal necrosis: Protein synthesis-independent activation of a cell death program

2003 ◽  
Vol 100 (5) ◽  
pp. 2825-2830 ◽  
Author(s):  
J. Niquet ◽  
R. A. Baldwin ◽  
S. G. Allen ◽  
D. G. Fujikawa ◽  
C. G. Wasterlain
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Neuronal Necrosis ◽  
Cell Death Program ◽  
A Cell

scholarly journals Heat stress induces ferroptosis in a photosynthetic prokaryote

2019 ◽  
Author(s):  
Anabella Aguilera ◽  
Federico Berdun ◽  
Carlos Bartoli ◽  
Charlotte Steelheart ◽  
Matías Alegre ◽  
...  
Keyword(s):  
Cell Death ◽  
Heat Stress ◽  
Similar Process ◽  
Cell Death Pathway ◽  
Regulated Cell Death ◽  
Cell Death Program ◽  
Dependent Form ◽  
A Cell ◽  
Eukaryotic Organisms ◽  
Pcc 6803

AbstractFerroptosis is an oxidative iron-dependent form of cell death recently described in eukaryotic organisms like animals, plants and parasites. Here we report that a similar process takes place in the cyanobacterium Synechocystis sp. PCC 6803 in response to heat stress. After a heat shock, Synechocystis cells undergo a cell death pathway that can be suppressed by canonical ferroptosis inhibitors or by external addition of calcium, glutathione or ascorbic acid. Moreover, as described for eukaryotic cells ferroptosis, this pathway is characterized by an early depletion of antioxidants, and by lipid peroxidation. As in general prokaryotes membranes contain poorly oxidizable saturated or monounsaturated lipid molecules, it was thought that they were not susceptible to ferroptosis. Interestingly, cyanobacteria contain thylakoid membranes that are enriched in polyunsaturated-fatty-acid-containing phospholipids, which might explain their sensitivity to ferroptosis. These results indicate that all of the hallmarks described for eukaryotic ferroptosis are conserved in photosynthetic prokaryotes and suggest that ferroptosis might be an ancient cell death program.SummaryAguilera et al, show that ferroptosis, an oxidative and iron-dependent form of regulated cell death, plays an important role in the cyanobacterium Synechocystis sp. PCC 6803 in response to heat stress.

scholarly journals Why yeast cells can undergo apoptosis: death in times of peace, love, and war

2006 ◽  
Vol 175 (4) ◽  
pp. 521-525 ◽  
Author(s):  
Sabrina Büttner ◽  
Tobias Eisenberg ◽  
Eva Herker ◽  
Didac Carmona-Gutierrez ◽  
Guido Kroemer ◽  
...  
Keyword(s):  
Cell Death ◽  
Single Cells ◽  
Yeast Cells ◽  
Unicellular Organism ◽  
Killer Toxins ◽  
Cell Biol ◽  
Cell Death Program ◽  
A Cell ◽  
Multicellular Organisms ◽  
Cell Suicide

The purpose of apoptosis in multicellular organisms is obvious: single cells die for the benefit of the whole organism (for example, during tissue development or embryogenesis). Although apoptosis has also been shown in various microorganisms, the reason for this cell death program has remained unexplained. Recently published studies have now described yeast apoptosis during aging, mating, or exposure to killer toxins (Fabrizio, P., L. Battistella, R. Vardavas, C. Gattazzo, L.L. Liou, A. Diaspro, J.W. Dossen, E.B. Gralla, and V.D. Longo. 2004. J. Cell Biol. 166:1055–1067; Herker, E., H. Jungwirth, K.A. Lehmann, C. Maldener, K.U. Frohlich, S. Wissing, S. Buttner, M. Fehr, S. Sigrist, and F. Madeo. 2004. J. Cell Biol. 164:501–507, underscoring the evolutionary benefit of a cell suicide program in yeast and, thus, giving a unicellular organism causes to die for.

C-ferroptosis is an iron-dependent form of regulated cell death in cyanobacteria

2021 ◽  
Vol 221 (2) ◽  
Author(s):  
Anabella Aguilera ◽  
Federico Berdun ◽  
Carlos Bartoli ◽  
Charlotte Steelheart ◽  
Matías Alegre ◽  
...  
Keyword(s):  
Cell Death ◽  
Similar Process ◽  
Cell Death Pathway ◽  
Regulated Cell Death ◽  
Cell Death Program ◽  
Dependent Form ◽  
A Cell ◽  
Eukaryotic Organisms ◽  
Synechocystis Sp ◽  
Pcc 6803

Ferroptosis is an oxidative and iron-dependent form of regulated cell death (RCD) recently described in eukaryotic organisms like animals, plants, and parasites. Here, we report that a similar process takes place in the photosynthetic prokaryote Synechocystis sp. PCC 6803 in response to heat stress. After a heat shock, Synechocystis sp. PCC 6803 cells undergo a cell death pathway that can be suppressed by the canonical ferroptosis inhibitors, CPX, vitamin E, Fer-1, liproxstatin-1, glutathione (GSH), or ascorbic acid (AsA). Moreover, as described for eukaryotic ferroptosis, this pathway is characterized by an early depletion of the antioxidants GSH and AsA, and by lipid peroxidation. These results indicate that all of the hallmarks described for eukaryotic ferroptosis are conserved in photosynthetic prokaryotes and suggest that ferroptosis might be an ancient cell death program.

scholarly journals Translation Inhibition by Rocaglates Activates a Species-Specific Cell Death Program in the Emerging Fungal Pathogen Candida auris

mBio ◽  
2020 ◽  
Vol 11 (2) ◽  
Author(s):  
Kali R. Iyer ◽  
Luke Whitesell ◽  
John A. Porco ◽  
Thomas Henkel ◽  
Lauren E. Brown ◽  
...  
Keyword(s):  
Cell Death ◽  
Translation Initiation ◽  
Fungal Pathogen ◽  
Initiation Factor ◽  
Candida Auris ◽  
Content Type ◽  
Translation Inhibition ◽  
Cell Death Program ◽  
A Cell ◽  
Species Specific

ABSTRACT Fungal infections are a major contributor to infectious disease-related deaths worldwide. Recently, global emergence of the fungal pathogen Candida auris has caused considerable concern because most C. auris isolates are resistant to fluconazole, the most commonly administered antifungal, and some isolates are resistant to drugs from all three major antifungal classes. To identify novel agents with bioactivity against C. auris, we screened 2,454 compounds from a diversity-oriented synthesis collection. Of the five hits identified, most shared a common rocaglate core structure and displayed fungicidal activity against C. auris. These rocaglate hits inhibited translation in C. auris but not in its pathogenic relative Candida albicans. Species specificity was contingent on variation at a single amino acid residue in Tif1, a fungal member of the eukaryotic initiation factor 4A (eIF4A) family of translation initiation factors known to be targeted by rocaglates. Rocaglate-mediated inhibition of translation in C. auris activated a cell death program characterized by loss of mitochondrial membrane potential, increased caspase-like activity, and disrupted vacuolar homeostasis. In a rocaglate-sensitized C. albicans mutant engineered to express translation initiation factor 1 (Tif1) with the variant amino acid that we had identified in C. auris, translation was inhibited but no programmed cell death phenotypes were observed. This surprising finding suggests divergence between these related fungal pathogens in their pathways of cellular responses to translation inhibition. From a therapeutic perspective, the chemical biology that we have uncovered reveals species-specific vulnerability in C. auris and identifies a promising target for development of new, mechanistically distinct antifungals in the battle against this emerging pathogen. IMPORTANCE Emergence of the fungal pathogen Candida auris has ignited intrigue and alarm within the medical community and the public at large. This pathogen is unusually resistant to antifungals, threatening to overwhelm current management options. By screening a library of structurally diverse molecules, we found that C. auris is surprisingly sensitive to translation inhibition by a class of compounds known as rocaglates (also known as flavaglines). Despite the high level of conservation across fungi in their protein synthesis machinery, these compounds inhibited translation initiation and activated a cell death program in C. auris but not in its relative Candida albicans. Our findings highlight a surprising divergence across the cell death programs operating in Candida species and underscore the need to understand the specific biology of a pathogen in attempting to develop more-effective treatments against it.

A Cell Death Pathway Induced by Antibody-Mediated Cross-Linking of CD45 on Lymphocytes

2003 ◽  
Vol 23 (5-6) ◽  
pp. 421-440 ◽  
Author(s):  
Ann-Muriel Steff ◽  
Marylene Fortin ◽  
Fabianne Philippoussis ◽  
Sylvie Lesage ◽  
Chantal Arguin ◽  
...  
Keyword(s):  
Cell Death ◽  
Cross Linking ◽  
Cell Death Pathway ◽  
A Cell

scholarly journals Translation machinery reprogramming in programmed cell death in Saccharomyces cerevisiae

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Francesco Monticolo ◽  
Emanuela Palomba ◽  
Maria Luisa Chiusano
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Acetic Acid ◽  
Programmed Cell Death ◽  
Differential Expression ◽  
Ribosomal Proteins ◽  
Relative Proportion ◽  
Duplication Event ◽  
Genome Duplication Event ◽  
Cell Death Pathway

AbstractProgrammed cell death involves complex molecular pathways in both eukaryotes and prokaryotes. In Escherichia coli, the toxin–antitoxin system (TA-system) has been described as a programmed cell death pathway in which mRNA and ribosome organizations are modified, favoring the production of specific death-related proteins, but also of a minor portion of survival proteins, determining the destiny of the cell population. In the eukaryote Saccharomyces cerevisiae, the ribosome was shown to change its stoichiometry in terms of ribosomal protein content during stress response, affecting the relative proportion between ohnologs, i.e., the couple of paralogs derived by a whole genome duplication event. Here, we confirm the differential expression of ribosomal proteins in yeast also during programmed cell death induced by acetic acid, and we highlight that also in this case pairs of ohnologs are involved. We also show that there are different trends in cytosolic and mitochondrial ribosomal proteins gene expression during the process. Moreover, we show that the exposure to acetic acid induces the differential expression of further genes coding for products related to translation processes and to rRNA post-transcriptional maturation, involving mRNA decapping, affecting translation accuracy, and snoRNA synthesis. Our results suggest that the reprogramming of the overall translation apparatus, including the cytosolic ribosome reorganization, are relevant events in yeast programmed cell death induced by acetic acid.

scholarly journals Mitochondria and Pharmacologic Cardiac Conditioning—At the Heart of Ischemic Injury

2021 ◽  
Vol 22 (6) ◽  
pp. 3224
Author(s):  
Christopher Lotz ◽  
Johannes Herrmann ◽  
Quirin Notz ◽  
Patrick Meybohm ◽  
Franz Kehl
Keyword(s):  
Cell Death ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition ◽  
Research Field ◽  
Calcium Handling ◽  
Control Mechanisms ◽  
Intrinsic Resistance ◽  
Atp Production ◽  
Cardiac Conditioning ◽  
A Cell

Pharmacologic cardiac conditioning increases the intrinsic resistance against ischemia and reperfusion (I/R) injury. The cardiac conditioning response is mediated via complex signaling networks. These networks have been an intriguing research field for decades, largely advancing our knowledge on cardiac signaling beyond the conditioning response. The centerpieces of this system are the mitochondria, a dynamic organelle, almost acting as a cell within the cell. Mitochondria comprise a plethora of functions at the crossroads of cell death or survival. These include the maintenance of aerobic ATP production and redox signaling, closely entwined with mitochondrial calcium handling and mitochondrial permeability transition. Moreover, mitochondria host pathways of programmed cell death impact the inflammatory response and contain their own mechanisms of fusion and fission (division). These act as quality control mechanisms in cellular ageing, release of pro-apoptotic factors and mitophagy. Furthermore, recently identified mechanisms of mitochondrial regeneration can increase the capacity for oxidative phosphorylation, decrease oxidative stress and might help to beneficially impact myocardial remodeling, as well as invigorate the heart against subsequent ischemic insults. The current review highlights different pathways and unresolved questions surrounding mitochondria in myocardial I/R injury and pharmacological cardiac conditioning.

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