Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA336005 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3991720.fastq.gz | Fastqsanger.gz | |||
| SRR3991721.fastq.gz | Fastqsanger.gz | |||
| SRR3991722.fastq.gz | Fastqsanger.gz | |||
| SRR3991723.fastq.gz | Fastqsanger.gz | |||
| SRR3991716.fastq.gz | Fastqsanger.gz |
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Project description:Understanding buffering mechanisms for various perturbations is essential for understanding robustness in cellular systems. Protein-level dosage compensation, which arises when changes in gene copy number do not translate linearly into protein level, is one mechanism for buffering against genetic perturbations. Here, we present an approach to identify genes with dosage compensation by increasing the copy number of individual genes using the genetic tug-of-war technique. Our screen of chromosome I suggests that dosage-compensated genes constitute approximately 10% of the genome and consist predominantly of subunits of multi-protein complexes. Importantly, because subunit levels are regulated in a stoichiometry-dependent manner, dosage compensation plays a crucial role in maintaining subunit stoichiometries. Indeed, we observed changes in the levels of a complex when its subunit stoichiometries were perturbed. We further analyzed compensation mechanisms using a proteasome-defective mutant as well as ribosome profiling, which provided strong evidence for compensation by ubiquitin-dependent degradation but not reduced translational efficiency. Thus, our study provides a systematic understanding of dosage compensation and highlights that this post-translational regulation is a critical aspect of robustness in cellular systems.
2016-12-30 | GSE85036 | GEO
Project description:Dosage compensation can buffer copy-number variation in wild yeast
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Project description:Dosage compensation can buffer copy-number variation in wild yeast
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Project description:Accurate prediction of cellular co-translational folding indicates proteins can switch from post- to co-translational folding
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Project description:To address the mechanisms of suppression, we analyzed time course of mRNA expression of four suppressed smc2-8 mutant strains. We addressed the question of genomic robustness by systematically screening genomic open reading frames, when induced for high-level expression, for their ability to suppress 55 conditional lethal mutations in yeast, and have discovered 636 suppressor genes participating in 822 novel dosage suppressor interactions. The suppressor genes are functionally broad and are enriched for overlapping open reading frames where mutually overlapping genes tend to be co-suppressors. Studies on suppressors of defects in chromosome condensation, telomere stability, and RNA polymerase II function suggest that adding interactions, by making significant connections where only weak or undetectable interactions were present (rewiring of gene regulatory pathways, and interaction within and between protein complexes) are frequent mechanisms of dosage suppression.
2011-09-21 | GSE24266 | GEO
Project description:Aneuploidy-induced proteotoxic stress can be effectively tolerated without dosage compensation, genetic mutations or stress responses
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Project description:Ras/cAMP signal transduction, perturbations
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Project description:Aneuploidy, the state in which an organism’s genome contains one or more missing or additional chromosomes, often causes widespread genotypic and phenotypic effects. Most often, aneuploidies are deleterious; the most common examples in humans being Down’s syndrome (Trisomy 21) and Turner’s syndrome (monosomy X). However, aneuploidy is surprisingly common in wild yeast populations. In recent years, there has been debate as to whether yeast contain an innate dosage compensation response on the whole-genome level, or if these natural isolates are robust to aneuploidy without such a mechanism. In this study, we tested for differential gene expression in 20 aneuploid and 18 euploid lines of yeast from two previous mutation accumulation experiments, where selection was low and therefore aneuploidies arose spontaneously. We found no evidence for whole-chromosome dosage compensation in aneuploid yeast but did find some evidence for attenuation of expression on a gene-by-gene basis. We additionally found that aneuploidy has no effect on the expression of the rest of the genome (i.e. “trans” genes), and that very few mutually exclusive aneuploid lines shared differentially expressed genes. However, we found a small common differential expression response in the euploid lines, suggesting an effect of mutation accumulation on gene expression. Our findings contribute to our understanding of aneuploidy in yeast and support the hypothesis that there is no innate dosage compensation mechanism at the whole-chromosome level.
2021-03-11 | GSE168674 | GEO
Project description:The Mediator complex transmits activation signals from DNA bound transcription factors to the core transcription machinery. Genome wide localization studies have demonstrated that Mediator occupancy not only correlates with high levels of transcription, but that the complex also is present at transcriptionally silenced locations. We provide evidence that Mediator localization is guided by an interaction with histone tails, and that this interaction is regulated by their post-translational modifications. A quantitative, high-density genetic interaction map revealed links between Mediator components and factors affecting chromatin structure, especially histone deacetylases. Peptide binding assays demonstrated that pure wild type Mediator forms stable complexes with the tails of Histone H3 and H4. These binding assays also showed Mediator – histone H4 peptide interactions are specifically inhibited by acetylation of the histone H4 lysine 16, a residue critical in transcriptional silencing. Finally, these findings were validated by tiling array analysis, that revealed a broad correlation between Mediator and nucleosome occupancy in vivo, but a negative correlation between Mediator and nucleosomes acetylated at histone H4 lysine 16. Our studies show that chromatin structure and the acetylation state of histones are intimately connected to Mediator localization.
2011-11-22 | GSE28613 | GEO
Project description:To address the mechanisms of suppression, we analyzed time course of mRNA expression of four suppressed smc2-8 mutant strains. We addressed the question of genomic robustness by systematically screening genomic open reading frames, when induced for high-level expression, for their ability to suppress 55 conditional lethal mutations in yeast, and have discovered 636 suppressor genes participating in 822 novel dosage suppressor interactions. The suppressor genes are functionally broad and are enriched for overlapping open reading frames where mutually overlapping genes tend to be co-suppressors. Studies on suppressors of defects in chromosome condensation, telomere stability, and RNA polymerase II function suggest that adding interactions, by making significant connections where only weak or undetectable interactions were present (rewiring of gene regulatory pathways, and interaction within and between protein complexes) are frequent mechanisms of dosage suppression. RNA samples isolated from two individual biological replicates, four time points each (0, 45, 90 and 180 min), of smc2-8 mutant strains harboring pGAL:SMC2, pGAL:UME1, pGAL:MEK1, pGAL:HTA2, pGAL:SNU66, and the negative control MORF plasmid (pGAL:negative, BG1766) and hybridized Affymetrix microarrays.
2011-09-20 | E-GEOD-24266 | biostudies-arrayexpress