scholarly journals Roles of the 2 microns gene products in stable maintenance of the 2 microns plasmid of Saccharomyces cerevisiae.

1987 ◽  
Vol 7 (10) ◽  
pp. 3566-3573 ◽  
Author(s):  
A E Reynolds ◽  
A W Murray ◽  
J W Szostak
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Copy Number ◽  
Gene Products ◽  
Site Specific ◽  
Cell Cycles ◽  
Daughter Cells ◽  
Repeat Sequences ◽  
Copy Numbers ◽  
Mother And Daughter ◽  
Stable Maintenance

We have examined the replication and segregation of the Saccharomyces cerevisiae 2 microns circle. The amplification of the plasmid at low copy numbers requires site-specific recombination between the 2 microns inverted repeat sequences catalyzed by the plasmid-encoded FLP gene. No other 2 microns gene products are required. The overexpression of FLP in a strain carrying endogenous 2 microns leads to uncontrolled plasmid replication, longer cell cycles, and cell death. Two different assays show that the level of Flp activity decreases with increasing 2 microns copy number. This regulation requires the products of the REP1 and REP2 genes. These gene products also act together to ensure that 2 microns molecules are randomly segregated between mother and daughter cells at cell division.

Roles of the 2 microns gene products in stable maintenance of the 2 microns plasmid of Saccharomyces cerevisiae

1987 ◽  
Vol 7 (10) ◽  
pp. 3566-3573
Author(s):  
A E Reynolds ◽  
A W Murray ◽  
J W Szostak
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Copy Number ◽  
Gene Products ◽  
Site Specific ◽  
Cell Cycles ◽  
Daughter Cells ◽  
Repeat Sequences ◽  
Copy Numbers ◽  
Mother And Daughter ◽  
Stable Maintenance

We have examined the replication and segregation of the Saccharomyces cerevisiae 2 microns circle. The amplification of the plasmid at low copy numbers requires site-specific recombination between the 2 microns inverted repeat sequences catalyzed by the plasmid-encoded FLP gene. No other 2 microns gene products are required. The overexpression of FLP in a strain carrying endogenous 2 microns leads to uncontrolled plasmid replication, longer cell cycles, and cell death. Two different assays show that the level of Flp activity decreases with increasing 2 microns copy number. This regulation requires the products of the REP1 and REP2 genes. These gene products also act together to ensure that 2 microns molecules are randomly segregated between mother and daughter cells at cell division.

scholarly journals Cell cycle phases in the unequal mother/daughter cell cycles of Saccharomyces cerevisiae.

1984 ◽  
Vol 4 (11) ◽  
pp. 2529-2531 ◽  
Author(s):  
B J Brewer ◽  
E Chlebowicz-Sledziewska ◽  
W L Fangman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cycle Phase ◽  
Cell Cycle Time ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cell Cycles ◽  
Daughter Cells ◽  
Mother And Daughter ◽  
Cell Cycle Phases ◽  
Mother Cells

During cell division in the yeast Saccharomyces cerevisiae mother cells produce buds (daughter cells) which are smaller and have longer cell cycles. We performed experiments to compare the lengths of cell cycle phases in mothers and daughters. As anticipated from earlier indirect observations, the longer cell cycle time of daughter cells is accounted for by a longer G1 interval. The S-phase and the G2-phase are of the same duration in mother and daughter cells. An analysis of five isogenic strains shows that cell cycle phase lengths are independent of cell ploidy and mating type.

Cell cycle phases in the unequal mother/daughter cell cycles of Saccharomyces cerevisiae

1984 ◽  
Vol 4 (11) ◽  
pp. 2529-2531
Author(s):  
B J Brewer ◽  
E Chlebowicz-Sledziewska ◽  
W L Fangman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Cycle Phase ◽  
Cell Cycle Time ◽  
Yeast Saccharomyces Cerevisiae ◽  
Cell Cycles ◽  
Daughter Cells ◽  
Mother And Daughter ◽  
Cell Cycle Phases ◽  
Mother Cells

During cell division in the yeast Saccharomyces cerevisiae mother cells produce buds (daughter cells) which are smaller and have longer cell cycles. We performed experiments to compare the lengths of cell cycle phases in mothers and daughters. As anticipated from earlier indirect observations, the longer cell cycle time of daughter cells is accounted for by a longer G1 interval. The S-phase and the G2-phase are of the same duration in mother and daughter cells. An analysis of five isogenic strains shows that cell cycle phase lengths are independent of cell ploidy and mating type.

scholarly journals Toxic effects of excess cloned centromeres.

1986 ◽  
Vol 6 (6) ◽  
pp. 2213-2222 ◽  
Author(s):  
B Futcher ◽  
J Carbon
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Copy Number ◽  
Spindle Pole Body ◽  
Spindle Pole ◽  
Host Cells ◽  
Selectable Markers ◽  
Pole Body ◽  
Copy Numbers ◽  
Yeast Plasmids

Plasmids carrying a Saccharomyces cerevisiae centromere have a copy number of one or two, whereas other yeast plasmids have high copy numbers. The number of CEN plasmids per yeast cell was made artificially high by transforming cells simultaneously with several different CEN plasmids carrying different, independently selectable markers. Some host cells carried five different CEN plasmids and an average total of 13 extra copies of CEN3. Several effects were noted. The copy number of each plasmid was unexpectedly high. The plasmids were mutually unstable. Cultures contained many dead cells. The viable host cells grew more slowly than control cells, even in nonselective medium. There was a pause in the cell cycle at or just before mitosis. We conclude that an excess of centromeres is toxic and that the copy number of centromere plasmids is low partly because of selection against cells carrying multiple centromere plasmids. The toxicity may be caused by competition between the centromeres for some factor present in limiting quantities, e.g., centromere-binding proteins, microtubules, or space on the spindle pole body.

scholarly journals The fitness cost of mismatch repair mutators in Saccharomyces cerevisiae: partitioning the mutational load

2019 ◽  
Author(s):  
Benjamin Galeota-Sprung ◽  
Breanna Guindon ◽  
Paul Sniegowski
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mismatch Repair ◽  
Separate Experiment ◽  
Mutational Load ◽  
Deleterious Mutations ◽  
Competitive Fitness ◽  
Daughter Cells ◽  
Point Estimates ◽  
Mother And Daughter ◽  
Mean Fitness

AbstractMutational load is the depression in a population’s mean fitness that results from the continual influx of deleterious mutations. Here, we directly estimate the mutational load in a population of haploid Saccharomyces cerevisiae that are deficient for mismatch repair. We partition the load in haploids into two components. To estimate the load due to nonlethal mutations, we measure the competitive fitness of hundreds of randomly selected clones from both mismatch repair-deficient and - proficient populations. Computation of the mean clone fitness for the mismatch repair-deficient strain permits an estimation of the nonlethal load, and the histogram of fitness provides an interesting visualization of a loaded population. In a separate experiment, in order to estimate the load due to lethal mutations (i.e. the lethal mutation rate), we manipulate thousands of individual pairs of mother and daughter cells and track their fates. These two approaches yield point estimates for the two contributors to load, and the addition of these estimates is nearly equal to the separately measured short-term competitive fitness deficit for the mismatch repair-deficient strain. This correspondence suggests that there is no need to invoke direct fitness effects to explain the fitness difference between mismatch repair-deficient and - proficient strains. Assays in diploids are consistent with deleterious mutations in diploids tending towards recessivity. These results enhance our understanding of mutational load, a central population genetics concept, and we discuss their implications for the evolution of mutation rates.

scholarly journals Aberrantly segregating centromeres activate the spindle assembly checkpoint in budding yeast.

1996 ◽  
Vol 133 (1) ◽  
pp. 75-84 ◽  
Author(s):  
W A Wells ◽  
A W Murray
Keyword(s):  
Copy Number ◽  
Spindle Assembly Checkpoint ◽  
Budding Yeast ◽  
Spindle Assembly ◽  
Pedigree Analysis ◽  
Eukaryotic Cells ◽  
Gene Products ◽  
Chromosome Behavior ◽  
Daughter Cells ◽  
Chromosome Alignment

The spindle assembly checkpoint is the mechanism or set of mechanisms that prevents cells with defects in chromosome alignment or spindle assembly from passing through mitosis. We have investigated the effects of mini-chromosomes on this checkpoint in budding yeast by performing pedigree analysis. This method allowed us to observe the frequency and duration of cell cycle delays in individual cells. Short, centromeric linear mini-chromosomes, which have a low fidelity of segregation, cause frequent delays in mitosis. Their circular counterparts and longer linear mini-chromosomes, which segregate more efficiently, show a much lower frequency of mitotic delays, but these delays occur much more frequently in divisions where the mini-chromosome segregates to only one of the two daughter cells. Using a conditional centromere to increase the copy number of a circular mini-chromosome greatly increases the frequency of delayed divisions. In all cases the division delays are completely abolished by the mad mutants that inactivate the spindle assembly checkpoint, demonstrating that the Mad gene products are required to detect the subtle defects in chromosome behavior that have been observed to arrest higher eukaryotic cells in mitosis.

scholarly journals SPOROGENIC ACTIVITIES OF MOTHER AND DAUGHTER CELLS IN SACCHAROMYCES CEREVISIAE

1970 ◽  
Vol 16 (4) ◽  
pp. 347-350 ◽  
Author(s):  
TOMOMICHI YANAGITA ◽  
MORIMASA YAGISAWA ◽  
SHINSHI OISHI ◽  
NOBUNDO SANDO ◽  
TSUNEJI SUTO
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Daughter Cells ◽  
Mother And Daughter

scholarly journals Active Stable Maintenance Functions in Low Copy-Number Plasmids of Gram-positive Bacteria. I. Partition Systems

2013 ◽  
Vol 62 (1) ◽  
pp. 3-16 ◽  
Author(s):  
MICHAŁ DMOWSKI ◽  
GRAŻYNA JAGURA-BURDZY
Keyword(s):  
Cell Division ◽  
Copy Number ◽  
Significant Contribution ◽  
Bacterial Cell Division ◽  
Gram Positive ◽  
Gram Positive Bacteria ◽  
Daughter Cells ◽  
Low Copy Number ◽  
Random Segregation ◽  
Stable Maintenance

Low copy number plasmids cannot rely on the random segregation during bacterial cell division. To be stably maintained in the population they evolved two types of mechanisms (i) partition systems (PAR) that actively separate replicated plasmid molecules to the daughter cells and (ii) toxin-andidote systems (TA) that act after cell division to kill plasmid-less cells. Our knowledge of partition systems has been based mainly on analysis of plasmids from Gram-negative bacteria. Now, numerous partition systems of plasmids from Gram-positive bacteria have also been characterized and make significant contribution to our understanding of these mechanisms.

scholarly journals Quantitative characterization of random partitioning in the evolution of plasmid-encoded traits

2019 ◽  
Author(s):  
Andrew D. Halleran ◽  
Emanuel Flores-Bautista ◽  
Richard M. Murray
Keyword(s):  
Copy Number ◽  
Plasmid Copy Number ◽  
Stochastic Simulations ◽  
Quantitative Characterization ◽  
Plasmid Copy ◽  
Daughter Cells ◽  
Copy Numbers ◽  
Plasmid Partitioning ◽  
Beneficial Allele

AbstractPlasmids are found across bacteria, archaea, and eukaryotes and play an important role in evolution. Plasmids exist at different copy numbers, the number of copies of the plasmid per cell, ranging from a single plasmid per cell to hundreds of plasmids per cell. This feature of a copy number greater than one can lead to a population of plasmids within a single cell that are not identical clones of one another, but rather have individual mutations that make a given plasmid unique. During cell division, this population of plasmids is partitioned into the two daughter cells, resulting in a random distribution of different plasmid variants in each daughter. In this study, we use stochastic simulations to investigate how random plasmid partitioning compares to a perfect partitioning model. Our simulation results demonstrate that random plasmid partitioning accelerates mutant allele fixation when the allele is beneficial and the selection is in an additive or recessive regime where increasing the copy number of the beneficial allele results in additional benefit for the host. This effect does not depend on the size of the benefit conferred or the mutation rate, but is magnified by increasing plasmid copy number.

scholarly journals The role of FIS in the Rcd checkpoint and stable maintenance of plasmid ColE1

Microbiology ◽  
2009 ◽  
Vol 155 (8) ◽  
pp. 2676-2682 ◽  
Author(s):  
I. K. Blaby ◽  
D. K. Summers
Keyword(s):  
Copy Number ◽  
Bacterial Population ◽  
Multicopy Plasmid ◽  
Concerted Action ◽  
Global Regulator ◽  
Synaptic Complex ◽  
Daughter Cells ◽  
Specific Manner ◽  
Stable Maintenance

Escherichia coli plasmid ColE1 lacks active partitioning, and copies are distributed randomly to daughter cells at division. The plasmid is maintained stably in the bacterial population as long as its copy number remains high. The accumulation of plasmid dimers and higher multimers depresses copy number, and is an important cause of multicopy plasmid instability. ColE1 dimers are restored to the monomeric state by site-specific recombination, which requires the host-encoded proteins XerCD, ArgR and PepA acting at the plasmid cer site. In addition, a 70 nt RNA expressed from the cer site of plasmid dimers delays the division of dimer-containing cells. Here, we report that the global regulator FIS binds to cer in a sequence-specific manner, close to the Rcd promoter (P cer ). FIS is not required for plasmid dimer resolution, but is essential for repression of P cer in plasmid monomers. Repression also requires the XerCD recombinase, but not ArgR or PepA. We propose a model for monomer–dimer control of P cer in which the promoter is repressed in plasmid monomers by the concerted action of FIS and XerCD. Rcd transcription is triggered in plasmid dimers by the lifting of XerCD-mediated repression in the synaptic complex.

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