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 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 An Upper Limit on the Functional Fraction of the Human Genome

2017 ◽  
Vol 9 (7) ◽  
pp. 1880-1885 ◽  
Author(s):  
Dan Graur
Keyword(s):  
Human Genome ◽  
Human Population ◽  
Mutational Load ◽  
Deleterious Mutations ◽  
Replacement Level ◽  
Functional Regions ◽  
Upper Limit ◽  
Constant Size ◽  
Mean Fitness ◽  
The Mean

AbstractFor the human population to maintain a constant size from generation to generation, an increase in fertility must compensate for the reduction in the mean fitness of the population caused, among others, by deleterious mutations. The required increase in fertility due to this mutational load depends on the number of sites in the genome that are functional, the mutation rate, and the fraction of deleterious mutations among all mutations in functional regions. These dependencies and the fact that there exists a maximum tolerable replacement level fertility can be used to put an upper limit on the fraction of the human genome that can be functional. Mutational load considerations lead to the conclusion that the functional fraction within the human genome cannot exceed 15%.

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.

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 Mutational Load and the Functional Fraction of the Human Genome

2020 ◽  
Vol 12 (4) ◽  
pp. 273-281 ◽  
Author(s):  
Benjamin Galeota-Sprung ◽  
Paul Sniegowski ◽  
Warren Ewens
Keyword(s):  
Human Genome ◽  
Practical Importance ◽  
Sequence Divergence ◽  
Mutational Load ◽  
Deleterious Mutations ◽  
Functional Sites ◽  
Large N ◽  
Systematic Effort ◽  
Selection Equilibrium ◽  
Mean Fitness

Abstract The fraction of the human genome that is functional is a question of both evolutionary and practical importance. Studies of sequence divergence have suggested that the functional fraction of the human genome is likely to be no more than ∼15%. In contrast, the ENCODE project, a systematic effort to map regions of transcription, transcription factor association, chromatin structure, and histone modification, assigned function to 80% of the human genome. In this article, we examine whether and how an analysis based on mutational load might set a limit on the functional fraction. In order to do so, we characterize the distribution of fitness of a large, finite, diploid population at mutation-selection equilibrium. In particular, if mean fitness is ∼1, the fitness of the fittest individual likely to occur cannot be unreasonably high. We find that at equilibrium, the distribution of log fitness has variance nus, where u is the per-base deleterious mutation rate, n is the number of functional sites (and hence incorporates the functional fraction f), and s is the selection coefficient of deleterious mutations. In a large (N=109) reproducing population, the fitness of the fittest individual likely to exist is ∼e5nus. These results apply to both additive and recessive fitness schemes. Our approach is different from previous work that compared mean fitness at mutation-selection equilibrium with the fitness of an individual who has no deleterious mutations; we show that such an individual is exceedingly unlikely to exist. We find that the functional fraction is not very likely to be limited substantially by mutational load, and that any such limit, if it exists, depends strongly on the selection coefficients of new deleterious mutations.

scholarly journals Mutational analysis of morphologic differentiation in Saccharomyces cerevisiae.

Genetics ◽  
1995 ◽  
Vol 140 (4) ◽  
pp. 1259-1275
Author(s):  
M J Blacketer ◽  
P Madaule ◽  
A M Myers
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mutational Analysis ◽  
Recessive Mutation ◽  
Daughter Cells ◽  
Affect Control ◽  
Mutant Strains ◽  
Growth Properties ◽  
Mother And Daughter ◽  
Multiple Characteristics ◽  
Agar Surface

Abstract A genetic analysis was undertaken to investigate the mechanisms controlling cellular morphogenesis in Saccharomyces cerevisiae. Sixty mutant strains exhibiting abnormally elongated cell morphology were isolated. The cell elongation phenotype in at least 26 of the strains resulted from a single recessive mutation. These mutations, designated generically elm (elongated morphology), defined 14 genes; two of these corresponded to the previously described genes GRR1 and CDC12. Genetic interactions between mutant alleles suggest that several ELM genes play roles in the same physiological process. The cell and colony morphology and growth properties of many elm mutant strains are similar to those of wild-type yeast strains after differentiation in response to nitrogen limitation into the pseudohyphal form. Each elm mutation resulted in multiple characteristics of pseudohyphal cells, including elongated cell shape, delay in cell separation, simultaneous budding of mother and daughter cells, a unipolar budding pattern, and/or the ability to grow invasively beneath the agar surface. Mutations in 11 of the 14 ELM gene loci potentiated pseudohyphal differentiation in nitrogen-limited medium. Thus, a subset of the ELM genes are likely to affect control or execution of a defined morphologic differentiation pathway in S. cerevisiae.

scholarly journals YeastMate: Neural network-assisted segmentation of mating and budding events in S. cerevisiae

2021 ◽  
Author(s):  
David Bunk ◽  
Julian Moriasy ◽  
Felix Thoma ◽  
Christopher Jakubke ◽  
Christof Osman ◽  
...  
Keyword(s):  
Neural Network ◽  
Saccharomyces Cerevisiae ◽  
Deep Learning ◽  
Source Code ◽  
Automated Detection ◽  
Daughter Cells ◽  
Mother And Daughter ◽  
User Friendly ◽  
Microscopy Images

Here, we introduce YeastMate, a user-friendly deep learning- based application for automated detection and segmentation of Saccharomyces cerevisiae cells and their mating and budding events in microscopy images. We build upon Mask R-CNN with a custom segmentation head for the subclassification of mother and daughter cells during lifecycle transitions. YeastMate can be used directly as a Python library or through a stand-alone GUI application and a Fiji plugin as easy to use frontends. The source code for YeastMate is freely available at https://github.com/hoerlteam/YeastMate under the MIT license. We offer packaged installers for our whole software stack for Windows, macOS and Linux. A detailed user guide is available at https://yeastmate.readthedocs.io.

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.

Chitin scar breaks in aged Saccharomyces cerevisiae

Microbiology ◽  
2003 ◽  
Vol 149 (11) ◽  
pp. 3129-3137 ◽  
Author(s):  
Chris D. Powell ◽  
David E. Quain ◽  
Katherine A. Smart
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Surface ◽  
Daughter Cell ◽  
Scar Tissue ◽  
Daughter Cells ◽  
Cell Age ◽  
Mother And Daughter ◽  
A Cell ◽  
Cell Surface Changes ◽  
Mother Cells

Ageing in budding yeast is not determined by chronological lifespan, but by the number of times an individual cell is capable of dividing, termed its replicative capacity. As cells age they are subject to characteristic cell surface changes. Saccharomyces cerevisiae reproduces asexually by budding and as a consequence of this process both mother and daughter cell retain chitinous scar tissue at the point of cytokinesis. Daughter cells exhibit a frail structure known as the birth scar, while mother cells display a more persistent bud scar. The number of bud scars present on the cell surface is directly related to the number of times a cell has divided and thus constitutes a biomarker for replicative cell age. It has been proposed that the birth scar may be subject to stretching caused by expansion of the daughter cell; however, no previous analysis of the effect of cell age on birth or bud scar size has been reported. This paper provides evidence that scar tissue expands with the cell during growth. It is postulated that symmetrically arranged breaks in the bud scar allow these rigid chitinous structures to expand without compromising cellular integrity.

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