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 The effect of oxygen concentration on the growth and metabolism of Saccharomyces cerevisiae grown with excess of potassium or in potassium-deficient media

1972 ◽  
Vol 130 (1) ◽  
pp. 251-258 ◽  
Author(s):  
Walter Bartley ◽  
Valerie M. Broomhead
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Death ◽  
Alcohol Dehydrogenase ◽  
Cytochrome Oxidase ◽  
Cell Size ◽  
Growth And Development ◽  
Yeast Cells ◽  
O2 Concentration ◽  
K Concentration ◽  
Effect Of Oxygen

1. Saccharomyces cerevisiae cells grown in limiting K+ concentration have their growth inhibited by O2 concentrations above 40%. With these conditions the cells grow very large and are unable to maintain ionic gradients when washed with water. 2. Cells grown in excess of K+ showed the same pattern of change in cell size with change in O2 concentration, but the magnitude of the changes was much less. Cells grown in excess of K+ were not leaky. 3. Cell death, growth and development of ‘leakiness’ were not correlated in the cells grown in limiting K+ concentration. 4. The activities of both alcohol dehydrogenase and cytochrome oxidase were higher in K+-deficient cells than in the cells grown with excess of K+. The differences were much larger when the measurements were made on a cellular basis than when made on a protein basis. 5. In 100% O2 3mm-K+ in the medium was sufficient to produce normal yeast cells.

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 Stable Pom1 clusters form a glucose-modulated concentration gradient that regulates mitotic entry

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Corey A H Allard ◽  
Hannah E Opalko ◽  
James B Moseley
Keyword(s):  
Cell Size ◽  
Concentration Gradient ◽  
Molecular Size ◽  
Yeast Cells ◽  
Small Cells ◽  
Cell Cortex ◽  
Mitotic Entry ◽  
Threshold Size ◽  
A Cell ◽  
Node Activation

Control of cell size requires molecular size sensors that are coupled to the cell cycle. Rod-shaped fission yeast cells divide at a threshold size partly due to Cdr2 kinase, which forms nodes at the medial cell cortex where it inhibits the Cdk1-inhibitor Wee1. Pom1 kinase phosphorylates and inhibits Cdr2, and forms cortical concentration gradients from cell poles. Pom1 inhibits Cdr2 signaling to Wee1 specifically in small cells, but the time and place of their regulatory interactions were unclear. We show that Pom1 forms stable oligomeric clusters that dynamically sample the cell cortex. Binding frequency is patterned into a concentration gradient by the polarity landmarks Tea1 and Tea4. Pom1 clusters colocalize with Cdr2 nodes, forming a glucose-modulated inhibitory threshold against node activation. Our work reveals how Pom1-Cdr2-Wee1 operates in multiprotein clusters at the cortex to promote mitotic entry at a cell size that can be modified by nutrient availability.

scholarly journals An AIF orthologue regulates apoptosis in yeast

2004 ◽  
Vol 166 (7) ◽  
pp. 969-974 ◽  
Author(s):  
Silke Wissing ◽  
Paula Ludovico ◽  
Eva Herker ◽  
Sabrina Büttner ◽  
Silvia M. Engelhardt ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Cyclophilin A ◽  
Yeast Cells ◽  
Mammalian Development ◽  
Oxygen Stress ◽  
A Cell ◽  
Death Effector ◽  
Induced Apoptosis ◽  
Apoptosis Inducing Factor

Apoptosis-inducing factor (AIF), a key regulator of cell death, is essential for normal mammalian development and participates in pathological apoptosis. The proapoptotic nature of AIF and its mode of action are controversial. Here, we show that the yeast AIF homologue Ynr074cp controls yeast apoptosis. Similar to mammalian AIF, Ynr074cp is located in mitochondria and translocates to the nucleus of yeast cells in response to apoptotic stimuli. Purified Ynr074cp degrades yeast nuclei and plasmid DNA. YNR074C disruption rescues yeast cells from oxygen stress and delays age-induced apoptosis. Conversely, overexpression of Ynr074cp strongly stimulates apoptotic cell death induced by hydrogen peroxide and this effect is attenuated by disruption of cyclophilin A or the yeast caspase YCA1. We conclude that Ynr074cp is a cell death effector in yeast and rename it AIF-1 (Aif1p, gene AIF1).

scholarly journals Regulation of Cell Size by Glucose Is Exerted via Repression of the CLN1 Promoter

1998 ◽  
Vol 18 (5) ◽  
pp. 2492-2501 ◽  
Author(s):  
Karin Flick ◽  
Daphne Chapman-Shimshoni ◽  
David Stuart ◽  
Marisela Guaderrama ◽  
Curt Wittenberg
Keyword(s):  
Cell Cycle ◽  
Cell Size ◽  
Transcriptional Repression ◽  
Yeast Cells ◽  
Glucose Addition ◽  
Cell Cycle Delay ◽  
Core Elements ◽  
Dependent Cell ◽  
A Cell

ABSTRACT Yeast cells are keenly sensitive to the availability and quality of nutrients. Addition of glucose to cells growing on a poorer carbon source elicits a cell cycle delay during G1 phase and a concomitant increase in the cell size. The signal is transduced through the RAS-cyclic AMP pathway. Using synchronized populations of G1 cells, we show that the increase in cell size required for budding depends upon CLN1 but not other G1 cyclins. This delay in cell cycle initiation is associated specifically with transcriptional repression of CLN1. CLN2 is not repressed. Repression of CLN1 is not limited to the first cycle following glucose addition but occurs in each cell cycle during growth on glucose. A 106-bp fragment of theCLN1 promoter containing the three MluI cell cycle box (MCB) core elements responsible for the majority ofCLN1-associated upstream activation sequence activity is sufficient to confer glucose-induced repression on a heterologous reporter. A mutant CLN2 promoter that is rendered dependent upon its three MCB core elements due to inactivation of its Swi4-dependent cell cycle box (SCB) elements is also repressed by glucose. The response to glucose is partially suppressed by inactivation of SWI4, but not MBP1, which is consistent with the dependence of MCB core elements upon the SCB-binding transcription factor (SBF). We suggest that differential regulation of CLN1 and CLN2 by glucose results from differences in the capacity of SBF to activate transcription driven by SCB and MCB core elements. Finally, we show that transcriptional repression is sufficient to explain the cell cycle delay that occurs in response to glucose.

scholarly journals The puc1 Cyclin Regulates the G1 Phase of the Fission Yeast Cell Cycle in Response to Cell Size

2000 ◽  
Vol 11 (2) ◽  
pp. 543-554 ◽  
Author(s):  
Cristina Martı́n-Castellanos ◽  
Miguel A. Blanco ◽  
José M. de Prada ◽  
Sergio Moreno
Keyword(s):  
Cell Cycle ◽  
Fission Yeast ◽  
Cell Size ◽  
Yeast Cells ◽  
G1 Phase ◽  
Close Relative ◽  
Cell Cycle Distribution ◽  
Cdk Inhibitor ◽  
Wild Type ◽  
A Cell

Eukaryotic cells coordinate cell size with cell division by regulating the length of the G1 and G2 phases of the cell cycle. In fission yeast, the length of the G1 phase depends on a precise balance between levels of positive (cig1, cig2, puc1, and cdc13 cyclins) and negative (rum1 and ste9-APC) regulators of cdc2. Early in G1, cyclin proteolysis and rum1 inhibition keep the cdc2/cyclin complexes inactive. At the end of G1, the balance is reversed and cdc2/cyclin activity down-regulates both rum1 and the cyclin-degrading activity of the APC. Here we present data showing that the puc1 cyclin, a close relative of the Cln cyclins in budding yeast, plays an important role in regulating the length of G1. Fission yeast cells lacking cig1 and cig2 have a cell cycle distribution similar to that of wild-type cells, with a short G1 and a long G2. However, when thepuc1 + gene is deleted in this genetic background, the length of G1 is extended and these cells undergo S phase with a greater cell size than wild-type cells. This G1 delay is completely abolished in cells lacking rum1. Cdc2/puc1 function may be important to down-regulate the rum1 Cdk inhibitor at the end of G1.

Spindle scaling mechanisms

2020 ◽  
Vol 64 (2) ◽  
pp. 383-396
Author(s):  
Lara K. Krüger ◽  
Phong T. Tran
Keyword(s):  
Cell Size ◽  
Spindle Assembly ◽  
Dependent Manner ◽  
Post Translational Modification ◽  
Size Dependent ◽  
A Cell ◽  
Chromosome Separation ◽  
Spindle Elongation ◽  
Protein Gradients ◽  
Spindle Structure

Abstract The mitotic spindle robustly scales with cell size in a plethora of different organisms. During development and throughout evolution, the spindle adjusts to cell size in metazoans and yeast in order to ensure faithful chromosome separation. Spindle adjustment to cell size occurs by the scaling of spindle length, spindle shape and the velocity of spindle assembly and elongation. Different mechanisms, depending on spindle structure and organism, account for these scaling relationships. The limited availability of critical spindle components, protein gradients, sequestration of spindle components, or post-translational modification and differential expression levels have been implicated in the regulation of spindle length and the spindle assembly/elongation velocity in a cell size-dependent manner. In this review, we will discuss the phenomenon and mechanisms of spindle length, spindle shape and spindle elongation velocity scaling with cell size.

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

Emulsion flow which preparation excludes a presence of mechanical impurities

2012 ◽  
Vol 9 (2) ◽  
pp. 118-122
Author(s):  
A.A. Rakhimov
Keyword(s):  
Cell Size ◽  
First Case ◽  
A Cell ◽  
Emulsion Flow ◽  
Blocking Mechanism

Experiments were carried out with waterhydrocarbon emulsions with various emulsifiers in capillaries with a length of 2 cm, diameters of 40 and 100 µm. To eliminate the influence of mechanical impurities comparable in size with the diameter of the capillary in first case emulsion components were filtered through fine-meshed filters. In second case obtained that way emulsion was additionally filtered through a system consisting of 3 filters with a cell size of 30-40 microns. In a capillary of 100 µm such emulsion came in a blocked state. Additional filtration of the emulsion through the mesh filters have led to an increase in viscosity but in 100 µm capillaries the time until the blocking 2-3 times more than the original. Rheology of used emulsions is well described by the model of Ostwald-de Waale. It was determined that emulsion blocking mechanism is due to the presence of inclusions not emulsion viscosity.

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