Comparative genomic hybridization of yeast strains with different chromosome copy numbers
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
SUBMITTER: Ariel Paulson
PROVIDER: E-MTAB-318 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Aneuploidy, the condition of having an abnormal number of chromosomes, is a hallmark of cancer cells. Recent work performed in yeast and mouse models suggests that aneuploidy interferes with cell proliferation and organism development. However, other recent experiments suggested that aneuploidy might play a positive role in tumor initiation and/or progression and in the emergence of chemotherapy as well as antibiotic resistances. Given its general deleterious effects on cellular fitness, how could aneuploidy be beneficial? In this set of experiments we plan to provide evidence that aneuploidy induces phenotypic variation through direct and indirect changes not only at the transcriptome but also at the proteome level.
2010-10-01 | E-MTAB-325 | biostudies-arrayexpress
Project description:In general, yeast strains with myo1 knocked out cannot perform cytokinesis, but some evolve new ways of accomplishing the task. This is an examination of aneuploidies and CNVs in a selection of evolved mutants that can successfully perform cytokinesis. The purpose is to attempt a molecular characterization of the evolved responses.
2008-11-24 | E-TABM-557 | biostudies-arrayexpress
Project description:There are many different types and origins of aneuploidy, but whether there is a uniform cellular response to aneuploidy in human cells has not been addressed so far. To uncover a uniform transcriptional response to aneuploidy we evaluted the transcription profiles of trisomic and tetrasomic cell lines and cell lines with complex aneuploid karyotypes. mRNA expression analysis of aneuploid cell lines derived from HCT116 compared to the HCT116 diploid cell line. With the exception of HCT116 3/3, three biological replicates of the Microarray experiment were performed.
2014-02-19 | E-GEOD-47830 | biostudies-arrayexpress
Project description:The replication of eukaryotic chromosomes is organized temporally and spatially within the nucleus through epigenetic regulation of replication origin function. The characteristic initiation timing of specific origins is thought to reflect their chromatin environment or sub-nuclear positioning, however the mechanism remains obscure. Here we show that the yeast Forkhead transcription factors, Fkh1 and Fkh2, are global determinants of replication origin timing. Forkhead regulation of origin timing is independent of local levels or changes of transcription. Instead, we show that Fkh1 and Fkh2 are required for the clustering of early origins and their association with the key initiation factor Cdc45 in G1-phase, suggesting that Fkh1 and Fkh2 selectively recruit origins to emergent replication factories. Fkh1 and Fkh2 bind Fkh-activated origins, and interact physically with ORC, providing a plausible mechanism to cluster origins. These findings add a new dimension to our understanding of the epigenetic basis for differential origin regulation and its connection to chromosomal domain organization. These files contain BrdU-IP-seq files (2 replicates for each strain; 5 strains total where WT was used as control). These files also contain RNA-seq data from Asynchronous and G1 arrested WT and Mutant cells (2 replicates per strain and condition; paired end). These files also contain RNA-pol-chip-seq data from Asynchronous and G1 arrested WT and Mutant cells (2 replicates per strain/condition).
2012-01-20 | E-GEOD-33677 | biostudies-arrayexpress
Project description:Cell division is a highly regulated process that secures the generation of healthy progeny in all organisms, from yeast to human. Dysregulation of this process can lead to uncontrolled cell proliferation and genomic instability, both which are hallmarks of cancer. Cell cycle progression is dictated by a complex network of kinases and phosphatases. These enzymes act on their substrates in a highly specific temporal manner ensuring that the process of cell division is unidirectional and irreversible. Key events of the cell cycle, such as duplication of genetic material and its redistribution to daughter cells, occur in S-phase and mitosis, respectively. Deciphering the dynamics of phosphorylation/dephosphorylation events during these cell cycle phases is important. Here we showcase a quantitative proteomic and phosphoproteomic mass spectrometry dataset that profiles both early and late phosphorylation events and associated proteome alterations that occur during S-phase and mitotic arrest in the model organism S. cerevisiae. This dataset is of broad interest as the molecular mechanisms governing cell cycle progression are conserved throughout evolution.
2022-09-02 | PXD035896 | Pride
Project description:Replication forks face multiple obstacles that slow their progression. By two-dimensional gel analysis, yeast forks pause at stable DNA protein complexes, and this pausing is greatly increased in the absence of the Rrm3 helicase. We used a genome wide approach to identify 96 sites of very high DNA polymerase binding in wild type cells. Most of these binding sites were not previously identified pause sites. Rather, the most highly represented genomic category among high DNA polymerase binding sites was the open reading frames (ORFs) of highly transcribed RNA polymerase II genes. Twice as many pause sites were identified in rrm3 compared to wild type cells as pausing in this strain occurred at both highly transcribed RNA polymerase II genes and the previously identified protein DNA complexes. ORFs of highly transcribed RNA polymerase II genes are the first class of natural pause sites that are not exacerbated in rrm3 cells. We alse mapped pause sites using a second replication fork component, Rrm3-13MYC and got similar results. Genomic input (labelled with Cy3) and IP'ed DNA (labelled with Cy5) using a MYC Ab of either DNA Pol2-13MYC or Rrm3-MYC from asynchronously grown S. cerevisiae cells in rich media were hybridized to whole-genome PCR-based arrays containing ORF and intergenic regions of the entire genome (Ivery et al 2001). At least three biological replication and one technical replicate (dye swap) were performed. Log2 transformed median normalized ratios (IP/IN) were averaged for each experiment and significant peaks of either DNA Pol2 or Rrm3 association were identified
2009-06-15 | E-GEOD-16218 | biostudies-arrayexpress
Project description:SSD1 is a polymorphic locus in budding yeast with many pleiotropic effects. Our lab had previously done transcript microarray of W303a in an ssd1-d background, and here we have carried out another transcript microarray across the cell cycle in an isogenic SSD1-V background. We find that a large fraction of budding yeast transcripts is differentially expressed in these cells. Ssd1 has recently been shown to bind mRNAs in vivo, but very few of these mRNAs show significant changes in levels in the SSD1-V versus ssd1-d comparison. About 20% of cell cycle-regulated transcripts are affected by SSD1-V and most of these transcripts show sharper amplitudes of oscillation in SSD1-V cells. Many transcripts whose gene products influence longevity are also affected, the largest class of which are involved in translation. Ribosomal protein mRNAs are globally down-regulated by SSD1-V. Cells were synchronized with alpha factor and sampled every 10 min across 2 cell cycles. A total of 13 samples were analyzed. No replicates were included. cDNA of the cell cycle samples were labelled with Cy5. For Cy3 labelling, asynchronous yeast population was used.
2010-05-06 | E-GEOD-16911 | biostudies-arrayexpress
Project description:We investigated how yeast cells deficient in performing homologous recombination-mediated DNA repair due to a deletion of the critical RAD52 gene respond to irreparable DNA damage inflicted by genotoxic treatment commonly applied in cancer therapy (camptothecin and irradiation). We found that upon persistence of irreparable DNA damage, yeast rad52 mutants readily undergo checkpoint adaptation accompanied by the acquisition of resistance to further genotoxic insults as well as the development of aneuploidy. Together, our findings can be used to elucidate how repair-defective cancer cells can become treatment-resistant thereby providing a way to target these resistant cell clones by tackling their aneuploidy-associated phenotypes. To investigate these characteristics commonly present in aneuploid cells in our experimental set-up, we treated yeast cells with genotoxic agents and performed whole genome sequencing. We could identify frequent whole chromosome loss events manifesting in a sensitivity of cells to aneuploidy-targeting agents.
2019-10-22 | E-MTAB-7380 | biostudies-arrayexpress
Project description:Candida albicans, the most common cause of human fungal infections, undergoes a reversible morphological transition from yeast to pseudohyphal and hyphal filaments, which is required for virulence. For many years, the relationship between global gene expression patterns associated with determination of specific C. albicans morphologies has remained obscure. Using a strain that can be genetically manipulated to sequentially transition from yeast to pseudohyphae to hyphae in the absence of complex environmental cues and upstream signaling pathways, we demonstrate by whole-genome transcriptional profiling that genes associated with pseudohyphae represent a subset of those associated hyphae and are generally expressed at lower levels; interestingly, no genes appeared to be expressed exclusively in pseudohyphae. Our results also strongly suggest that in addition to dosage, extended duration of filament-specific gene expression is sufficient to drive the C. albicans yeast-pseudohyphal-hyphal transition. Finally, we describe the first transcriptional profile of the C. albicans reverse hyphal-pseudohyphal-yeast transition and demonstrate that this transition not only involves down-regulation of known hyphal-specific genes but also differential expression of additional genes which have not previously been associated with the forward transition, including many involved in protein synthesis. These findings provide new insight into genome-wide mechanisms important for determining fungal morphology and suggest that in addition to similarities, there are also fundamental differences in global gene expression as pathogenic filamentous fungi undergo forward and reverse morphological transitions. The Dosage Experiment (13 arrays) was performed twice (two biological replicates). MBY38 cells were treated with various concentrations of Doxycycline (Dox): 20 (n=3), 0.4 (n=1), 0.35 (n=1), 0.3 (n=1), 0.25 (n=1), 0.2 (n=1), 0.15 (n=1), 0.1 (n=1), 0.05 (n=1), 0.02 (n=1) and 0 µg/mL (n=1). Each 20 ug/ml sample was used for 3 technical replicate arrays, one of which was labeled using reverse fluors. The reference sample consisted of equal aliquots of the experimental samples. The Forward Transition Experiment (23 arrays) was performed twice (two biological replicates). MBY38 cells were grown in the presence (n=10) or absence (n=10) of 1.0 ug/ml Dox and subsequently harvested at time points between 1 and 10 hours. Each 1.0 ug/mL Dox treated sample was collected at 0 hours and used for 3 technical replicate arrays, one of which was labeled using reverse fluors. The reference sample consisted of equal aliquots of all 21 experimental samples. The Reverse Transition Experiment (26 arrays) was performed twice (two biological replicates). MBY38 cells were grown in the presence (n=10) or absence (n=10) of 20.0 ug/ml Dox and subsequently harvested at time points between 1 and 10 hours. Each 20.0 ug/mL sample was collected at 0 hours and used for 3 technical replicate arrays, one of which was labeled using reverse fluors. Each untreated (no Dox) sample was collected at 0 hours and used for 3 technical replicate arrays, one of which was labeled using reverse fluors. The reference sample consisted of equal aliquots of all 22 experimental samples. The Dox Control Experiment consisted of 12 arrays. PCY87 cells were grown in the presence (n=5) or absence (n=5) of 20.0 ug/ml Dox overnight to create 5 pairs of biological replicates. Three pairs of biological replicates were labelled normally (one of which was repeated as a technical replicate using reverse fluors) and 2 pairs of biological replicates were labeled using reverse fluors. The Dosage Experiment reference was used as the reference sample.
2012-12-12 | E-GEOD-39677 | biostudies-arrayexpress
Project description:During translation elongation, the ribosome ratchets along its mRNA template, incorporating each new amino acid and translocating from one codon to the next. The elongation cycle requires dramatic structural rearrangements of the ribosome. We show here that deep sequencing of ribosome-protected mRNA fragments reveals not only the position of each ribosome but also, unexpectedly, its particular stage of the elongation cycle. Sequencing reveals two distinct populations of ribosome footprints, 28-30 nucleotides and 20-22 nucleotides long, representing translating ribosomes in distinct states, differentially stabilized by specific elongation inhibitors. We find that the balance of small and large footprints varies by codon and is correlated with translation speed. The ability to visualize conformational changes in the ribosome during elongation, at single-codon resolution, provides a new way to study the detailed kinetics of translation and a new probe with which to identify the factors that affect each step in the elongation cycle. Ribosome profiling, or sequencing of ribosome-protected mRNA fragments, in yeast. We assay ribosome footprint sizes and positions in three conditions: untreated yeast (3 replicates) and yeast treated with translation inhibitors cycloheximide (2 replicates) and anisomycin (2 biological replicates, one technical replicate). We also treat yeast with 3-aminotriazole to measure the effect of limited histidine tRNAs on ribosome footprint size and distribution (two treatment durations).
2014-06-10 | E-GEOD-58321 | biostudies-arrayexpress