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.

scholarly journals Chronological aging leads to apoptosis in yeast

2004 ◽  
Vol 164 (4) ◽  
pp. 501-507 ◽  
Author(s):  
Eva Herker ◽  
Helmut Jungwirth ◽  
Katharina A. Lehmann ◽  
Corinna Maldener ◽  
Kai-Uwe Fröhlich ◽  
...  
Keyword(s):  
Apoptotic Cell ◽  
Selective Advantage ◽  
Yeast Cells ◽  
Unicellular Organism ◽  
Chronological Aging ◽  
Beneficial Effects ◽  
Yeast Cultures ◽  
A Cell ◽  
Cell Suicide

During the past years, yeast has been successfully established as a model to study mechanisms of apoptotic regulation. However, the beneficial effects of such a cell suicide program for a unicellular organism remained obscure. Here, we demonstrate that chronologically aged yeast cultures die exhibiting typical markers of apoptosis, accumulate oxygen radicals, and show caspase activation. Age-induced cell death is strongly delayed by overexpressing YAP1, a key transcriptional regulator in oxygen stress response. Disruption of apoptosis through deletion of yeast caspase YCA1 initially results in better survival of aged cultures. However, surviving cells lose the ability of regrowth, indicating that predamaged cells accumulate in the absence of apoptotic cell removal. Moreover, wild-type cells outlast yca1 disruptants in direct competition assays during long-term aging. We suggest that apoptosis in yeast confers a selective advantage for this unicellular organism, and demonstrate that old yeast cells release substances into the medium that stimulate survival of the clone.

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 Cell Size Influences the Reproductive Potential and Total Lifespan of theSaccharomyces cerevisiaeYeast as Revealed by the Analysis of Polyploid Strains

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Renata Zadrag-Tecza ◽  
Magdalena Kwolek-Mirek ◽  
Małgorzata Alabrudzińska ◽  
Adrianna Skoneczna
Keyword(s):  
Cell Death ◽  
Cell Size ◽  
Reproductive Potential ◽  
Threshold Value ◽  
Yeast Cells ◽  
Common Mechanism ◽  
A Cell ◽  
Genome Copy Number ◽  
The Difference ◽  
Two Phases

The total lifespan of the yeastSaccharomyces cerevisiaemay be divided into two phases: the reproductive phase, during which the cell undergoes mitosis cycles to produce successive buds, and the postreproductive phase, which extends from the last division to cell death. These phases may be regulated by a common mechanism or by distinct ones. In this paper, we proposed a more comprehensive approach to reveal the mechanisms that regulate both reproductive potential and total lifespan in cell size context. Our study was based on yeast cells, whose size was determined by increased genome copy number, ranging from haploid to tetraploid. Such experiments enabled us to test the hypertrophy hypothesis, which postulates that excessive size achieved by the cell—the hypertrophy state—is the reason preventing the cell from further proliferation. This hypothesis defines the reproductive potential value as the difference between the maximal size that a cell can reach and the threshold value, which allows a cell to undergo its first cell cycle and the rate of the cell size to increase per generation. Here, we showed that cell size has an important impact on not only the reproductive potential but also the total lifespan of this cell. Moreover, the maximal cell size value, which limits its reproduction capacity, can be regulated by different factors and differs depending on the strain ploidy. The achievement of excessive size by the cell (hypertrophic state) may lead to two distinct phenomena: the cessation of reproduction without “mother” cell death and the cessation of reproduction with cell death by bursting, which has not been shown before.

scholarly journals Human Bak induces cell death in Schizosaccharomyces pombe with morphological changes similar to those with apoptosis in mammalian cells.

1997 ◽  
Vol 17 (5) ◽  
pp. 2468-2474 ◽  
Author(s):  
B Ink ◽  
M Zörnig ◽  
B Baum ◽  
N Hajibagheri ◽  
C James ◽  
...  
Keyword(s):  
Cell Death ◽  
Schizosaccharomyces Pombe ◽  
Mammalian Cells ◽  
Morphological Changes ◽  
Yeast Cells ◽  
Bh3 Domain ◽  
Evolutionarily Conserved ◽  
Unicellular Organisms ◽  
Induction Of Apoptosis ◽  
Multicellular Organisms

Apoptosis as a form of programmed cell death (PCD) in multicellular organisms is a well-established genetically controlled process that leads to elimination of unnecessary or damaged cells. Recently, PCD has also been described for unicellular organisms as a process for the socially advantageous regulation of cell survival. The human Bcl-2 family member Bak induces apoptosis in mammalian cells which is counteracted by the Bcl-x(L) protein. We show that Bak also kills the unicellular fission yeast Schizosaccharomyces pombe and that this is inhibited by coexpression of human Bcl-x(L). Moreover, the same critical BH3 domain of Bak that is required for induction of apoptosis in mammalian cells is also required for inducing death in yeast. This suggests that Bak kills mammalian and yeast cells by similar mechanisms. The phenotype of the Bak-induced death in yeast involves condensation and fragmentation of the chromatin as well as dissolution of the nuclear envelope, all of which are features of mammalian apoptosis. These data suggest that the evolutionarily conserved metazoan PCD pathway is also present in unicellular yeast.

scholarly journals Cell explosions: single cell death triggers an avoidance response in local populations of the ecologically prominent phytoplankton genus Micromonas

2019 ◽  
Author(s):  
Richard Henshaw ◽  
Jonathan Roberts ◽  
Marco Polin
Keyword(s):  
Cell Death ◽  
Avoidance Response ◽  
Single Cell ◽  
Single Cells ◽  
Local Environment ◽  
Warning Signal ◽  
Predator Prey ◽  
A Cell ◽  
Observed Behaviour ◽  
Micromonas Pusilla

The global phytoplankton community, comprised of aquatic photosynthetic organisms, is acknowledged for being responsible for half of the global oxygen production Prominent among these is the pico-eukaryote Micromonas commoda (formally Micromonas pusilla of the genus Micromonas), which can be found in marine and coastal environments across the globe. Cell death of phytoplankton has been identified as contributing to the largest carbon transfers on the planet moving 109 tonnes of carbon in the oceans every day. During a cell death organic matter is released into the local environment which can act as both a food source and a warning signal for nearby organisms. Here we present a novel motility response to single cell death in populations of Micromonas sp., where the death of a single cell releases a chemical patch triggers surrounding cells to escape the immediate affected area. These so-called “burst events” are then modelled and compared with a spherically symmetric diffusing patch which is found to faithfully reproduce the observed behaviour. Finally, laser ablation of single cells reproduces the observed avoidance response, confirming that Micromonas sp. has evolved a specific motility response in order to escape harmful environments for example nearby predator-prey interactions or virus lysis induced cell death.

scholarly journals Autophagy and cell death: The jury's still out

2012 ◽  
Vol 34 (2) ◽  
pp. 14-19
Author(s):  
Jon D. Lane ◽  
Virginie M.S. Betin ◽  
Lilith Mannack ◽  
Tom D.B. MacVicar
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Mammalian Cells ◽  
Autophagic Cell Death ◽  
Circumstantial Evidence ◽  
Innocent Bystander ◽  
Catastrophic Loss ◽  
A Cell ◽  
Cell Suicide ◽  
Timely Death

Since the publication of seminal work in the early 1970s by John Kerr and Andrew Wyllie1, we have been aware that mammalian cells have the genetically encoded capability to give up the ghost and trigger a highly conserved cell-suicide pathway called apoptosis. Not content with this important knowledge, many researchers have spent the intervening years attempting to identify and characterize other ‘programmed cell death’ (PCD) mechanisms that might also have important roles in development and disease. One of these was ‘autophagy’, a process by which cells became vacuolated and progressively devoid of cytoplasm. Over the years, ‘autophagic cell death’ has been linked with the timely death of cells in development, as well as the catastrophic loss of cells in several important human diseases. But is autophagy truly a cell death mechanism in its own right? Perhaps it is just an innocent bystander, unfairly accused on the basis of flimsy circumstantial evidence? The jury may finally be poised to return a decisive verdict….

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 Oncogenic Ras triggers cell suicide through the activation of a caspase-independent cell death program in human cancer cells

Oncogene ◽  
1999 ◽  
Vol 18 (13) ◽  
pp. 2281-2290 ◽  
Author(s):  
Shunji Chi ◽  
Chifumi Kitanaka ◽  
Kohji Noguchi ◽  
Toshihiro Mochizuki ◽  
Yohji Nagashima ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Human Cancer ◽  
Human Cancer Cells ◽  
Oncogenic Ras ◽  
Cell Death Program ◽  
Cell Suicide

scholarly journals ‘Bacterial Programmed Cell Death’: cellular altruism or genetic selfism?

2020 ◽  
Vol 367 (16) ◽  
Author(s):  
Bhaskar Chandra Mohan Ramisetty ◽  
Pavithra Anantharaman Sudhakari
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Free Living ◽  
Selfish Genes ◽  
A Cell ◽  
Unicellular Organisms ◽  
Multicellular Organisms ◽  
Restriction Modification ◽  
Restriction Modification Systems ◽  
Selection Of

ABSTRACT Cell-dependent propagation of the ‘self’ is the driver of all species, organisms and even genes. Conceivably, elimination of these entities is caused by cellular death. Then, how can genes that cause the death of the same cell evolve? Programmed cell death (PCD) is the gene-dependent self-inflicted death. In multicellular organisms, PCD of a cell confers fitness to the surviving rest of the organism, which thereby allows the selection of genes responsible for PCD. However, PCD in free-living bacteria is intriguing; the death of the cell is the death of the organism. How can such PCD genes be selected in unicellular organisms? The bacterial PCD in a population is proposed to confer fitness to the surviving kin in the form of sporulation, nutrition, infection-containment and matrix materials. While the cell-centred view leading to propositions of ‘altruism’ is enticing, the gene-centred view of ‘selfism’ is neglected. In this opinion piece, we reconceptualize the PCD propositions as genetic selfism (death due to loss/mutation of selfish genes) rather than cellular altruism (death for the conferment of fitness to kin). Within the scope and the available evidence, we opine that some of the PCD-like observations in bacteria seem to be the manifestation of genetic selfism by Restriction–Modification systems and Toxin–Antitoxin systems.

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