Mutation accumulation and the yeast transcriptome
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE7537 | GEO | 2007/06/01
SECONDARY ACCESSION(S): PRJNA99365
REPOSITORIES: GEO
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Project description:45 genome-wide microarray measurements for 23 mutation accumulation lines grown in YPD liquid culture MA lines obtained by single-colony transfer on YPD plates for 600 generations, starting from a BY4741 derived strain (see Zeyl C, DeVisser JA: Estimates of the rate and distribution of fitness effects of spontaneous mutation in Saccharomyces cerevisiae. Genetics 2001, 157:53–61)
2010-10-19 | GSE24770 | GEO
Project description:45 genome-wide microarray measurements for 23 mutation accumulation lines grown in YPD liquid culture MA lines obtained by single-colony transfer on YPD plates for 600 generations, starting from a BY4741 derived strain (see Zeyl C, DeVisser JA: Estimates of the rate and distribution of fitness effects of spontaneous mutation in Saccharomyces cerevisiae. Genetics 2001, 157:53â61) Two biological replicates for each strain in a common reference design (no dye-swap)
2010-10-19 | E-GEOD-24770 | biostudies-arrayexpress
Project description:Haploid, diploid, and tetraploid yeast were experimentally evolved in 2% raffinose medium. After 250 generations, we assessed the gene expression alterations in 2 evolved haploids, 2 evolved diploids, and 4 evolved tetraploids relative to the diploid ancestor.
2017-10-04 | GSE95069 | GEO
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Project description:Adaptive evolution is generally assumed to progress through the accumulation of beneficial mutations. However, deleterious mutations may also have an important role by promoting adaptive genetic changes that are otherwise inaccessible. Here we study the capacity of the bakerM-bM-^@M-^Ys yeast genome to compensate the complete loss of genes during evolution, and explore the long-term consequences of this process. We initiated laboratory evolutionary experiments with over 180 haploid yeast genotypes, all of which initially displayed slow growth due to the deletion of a single gene. Compensatory adaptation was rapid and pervasive, and it promoted the genomic divergence of parallel evolving populations. The accumulated mutations did not restore wild type genomic expression states and generated diverse growth phenotypes across environments. Taken together, gene loss initiates genomic changes that can influence evolutionary potential upon environmental change. Evolved yeast-lines were generated by growing strains for 400 doublings during 104 days on YPD medium in 96 wells plates, 8 evolved lines were selected for microarray analysis. Two independent colonies of the wild type control, evolved and corresponding ancestor knock-out strains were grown to early midlog and used for transcription profiling by dual channel array against a common reference.
2014-08-27 | E-GEOD-55373 | biostudies-arrayexpress
Project description:Gene expression profiling revealed that hundreds of genes were differentially expressed among these Y introgression lines, and that global gene expression pattern diverged between the low-PEV and high-PEV (defined in the accompanying publication) flies. The results further expand our understanding of the role of the Y chromosome in modulating global gene expression, and suggest a link with modifications of chromatin state. Keywords: position-effect variegation (PEV) The Y chromosomes of H15 and H23 have lower level of suppression on the expression of white gene, therefore show lower level of eye color variegation. In contrast, the Y chromosomes of H5 and H7 have higher level of suppression on the expression of white gene resulting higher level of eye variegation. A loop design was used with all the Y introgression lines. In addition to biological replicates, a Cy5-Cy3 dye swap was performed.
2012-04-04 | E-GEOD-37068 | biostudies-arrayexpress
Project description:The experimental evolution of laboratory populations of microbes provides an opportunity to observe the evolutionary dynamics of adaptation in real time.Until very recently, however, such studies have been limited by our inability to systematically find mutations in evolved organisms.We overcome this limitation by using a variety of DNA microarray-based techniques to characterize genetic changes, including point mutations, structural changes, and insertion variation, that resulted from the experimental adaptation of 24 haploid and diploid cultures of Saccharomyces cerevisiae to growth in glucose-, sulfate, or phosphate-limited chemostats for ~ 200 generations.We identified frequent genomic amplifications and rearrangements as well as novel retrotransposition events associated with adaptation.Global mutation detection in 10 clonal isolates identified 32 point mutations. On the basis of mutation frequencies, we infer that these mutations and the subsequent dynamics of adaptation are determined by the batch phase of growth prior to initiation of continuous phase in the chemostat.We relate these genotypic changes to phenotypic outcomes, namely global patterns of gene expression, and to increases in fitness by 5-50%. We found that the spectrum of available mutations in glucose or phosphate-limited environments combined with the batch phase population dynamics early in our experiments to allow several distinct genotypic and phenotypic evolutionary pathways in response to these nutrient limitations. By contrast, sulfate-limited populations were much more constrained in both genotypic and phenotypic outcomes.Thus, the reproducibility of evolution varies with specific selective pressures reflecting the constraints inherent in the system-level organization of metabolic processes in the cell.We were able to relate some of the observed adaptive mutations (e.g. transporter gene amplifications) to known features of the relevant metabolic pathways, but many of the mutations pointed to genes not previously associated with the relevant physiology. Thus, in addition to answering basic mechanistic questions about evolutionary mechanisms our work suggests that experimental evolution can also shed light on the function and regulation of individual metabolic pathways. Keywords: gene expression, CGH, and TSE analysis consult individual records for details of analysis This Dataset consists of several experiments: Gene expression experiments found in Figure 1a of paper: Design: RNA from each evolved clone or population grown in chemostat culture is compared to RNA from matching ancestor strains grown in the same conditions. Samples: GSM339025-GSM339088 CGH experiments found in Figure 2A, Figure 3, and Table S2: Experiment design: DNA from each evolved clone or population is hybridized vs DNA from the matched ancestor strain Samples: GSM339089-GSM339146 CGH experiments found in Table S3: Experiment design: DNA from each segregant derived from an evolved strain is hybridized vs DNA from the matched ancestor strain Samples: GSM339147-GSM339158 Gel band CGH experiments found in Figure S1: Experiment design: Chromosomes from evolved strains were run on a gel and excised. DNA from the bands is hybridized vs matched ancestor genomic DNA Samples: GSM339159-GSM339184 TSE CGH experiments found in Table S4: Experiment design: DNA linked to Ty1/Ty2 sequences was extracted from evolved strains and ancestor strains, and compared to ancestral extracted or genomic DNA as indicated. Samples: GSM339185-GSM339212 CGH experiments for experiments in Figure S7: Experiment design: DNA from 2 strains transformed with a SUL1 plasmid hybridized vs DNA from the matched ancestor strain Samples: GSM339213 and GSM339214
2010-05-18 | E-GEOD-13435 | biostudies-arrayexpress
Project description:Analysis of copy number variation in evolved haploid, diploid, tetraploid strains.
2015-02-28 | GSE51017 | GEO
Project description:microarray experiment to test the gene expression in long term lines of mutator and non-mutator yeast. Here we use an experimental evolution approach to investigate the conditions required for evolution of a reduction in mutation rate and the mechanisms by which populations tolerate the accumulation of deleterious mutations. We find that after ~6700 generations four out of eight experimental mutator lines had evolved a decreased mutation rate. 2 condition experiment, derived experimental evolution strains compared to their ancestor strain. We compared the expression profile of one of the mutator lines (m8) after 6700 generations with its mutator ancestor, and as a control, an evolved non mutator after 6700 generations was compared to to its non-mutator ancestor. In order to prepare cells for expression microarray, glass tubes containing 3 ml of YPD were inoculated from overnight cultures, and grown until the OD600 was approximately 0.3.
2012-02-02 | E-GEOD-35440 | biostudies-arrayexpress
Project description:Mutations accumulate within somatic cells and have been proposed to contribute to aging. It is unclear what level of mutation burden may be required to consistently reduce cellular lifespan. Human cancers driven by a mutator phenotype represent an intriguing model to test this hypothesis, since they carry the highest mutation burdens of any human cell. However, it remains technically challenging to measure the replicative lifespan of individual mammalian cells. Here, we modeled the consequences of cancer-related mutator phenotypes on lifespan using yeast defective for mismatch repair (MMR) and/or leading strand (Polε) or lagging strand (Polδ) DNA polymerase proofreading. Only haploid mutator cells with significant lifetime mutation accumulation (MA) exhibited shorter lifespans. Diploid strains, derived by mating haploids of various genotypes, carried variable numbers of fixed mutations and a range of mutator phenotypes. Some diploid strains with fewer than two mutations per megabase displayed a 25% decrease in lifespan, suggesting that moderate numbers of random heterozygous mutations can increase mortality rate. As mutation rates and burdens climbed, lifespan steadily eroded. Strong diploid mutator phenotypes produced a form of genetic anticipation with regard to aging, where the longer a lineage persisted, the shorter lived cells became. Using MA lines, we established a relationship between mutation burden and lifespan, as well as population doubling time. Our observations define a threshold of random mutation burden that consistently decreases cellular longevity in diploid yeast cells. Many human cancers carry comparable mutation burdens, suggesting that while cancers appear immortal, individual cancer cells may suffer diminished lifespan due to accrued mutation burden.
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