Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA476856 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7446240_1.fastq.gz | Fastqsanger.gz | |||
| SRR7446240_2.fastq.gz | Fastqsanger.gz | |||
| SRR7446250.fastq.gz | Fastqsanger.gz | |||
| SRR7446260_1.fastq.gz | Fastqsanger.gz | |||
| SRR7446260_2.fastq.gz | Fastqsanger.gz |
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Project description:Two models have been put forward for cyclin-dependent kinase (Cdk) control of the cell cycle. In the qualitative model, cell cycle events are ordered by distinct substrate specificities associated with successive waves of G1, S and mitotic cyclins. Alternatively, the gradual quantitative rise of Cdk activity from G1 phase to mitosis could lead to ordered substrate phosphorylation at sequential thresholds. Here, we study the relative contributions of qualitative and quantitative Cdk control in the budding yeast S. cerevisiae. S-phase cyclins can be replaced by a single mitotic cyclin, albeit at the cost of reduced fitness. The single cyclin can in addition replace G1 cyclins to support ordered cell cycle progression, fulfilling key predictions of the quantitative model. However, single-cyclin cells fail to polarize or grow buds and thus cannot sustain proliferation. Our results suggest that budding yeast has become dependent on G1 cyclin specificity to couple cell cycle progression to essential morphogenetic events.
2021-08-23 | PXD022757 | Pride
Project description:Yeast cell cycle transcription dynamics in two S. cerevisae strains: BF264-15DU (MATa ade1 his2 leu2-3, 112 trp1-1 ura3Dns, bar1) [referred to as wild type] and a mutant of the wild type strain, clb1,2,3,4,5,6 GAL1-CLB1, [referred to as cyclin mutant] that does not express S-phase and mitotic cyclins. Both strains were synchronized by elutriation and released into YEP 2% dextrose/1M sorbitol at 30c. 15 samples were taken at 16 min intervals covering ~2 cycles in wild-type and ~1.5 cycles for the mutants. A significant fraction of the Saccharomyces cerevisiae genome is transcribed periodically during the cell division cycle, suggesting that properly timed gene expression is important for regulating cell cycle events. Genomic analyses of transcription factor localization and expression dynamics suggest that a network of sequentially expressed transcription factors could control the temporal program of transcription during the cell cycle. However, directed studies interrogating small numbers of genes indicate that their periodic transcription is governed by the activity of cyclin-dependent kinases (CDKs). To determine the extent to which the global cell cycle transcription program is controlled by cyclin/CDK complexes, we compared genome-wide transcription dynamics in wild type budding yeast to mutants that do not express S-phase and mitotic cyclins. Experiment Overall Design: Cell cycle synchrony/time series experiments. G1 cells collected by elutriation was examined over time for 2 cell cycles. Strains compared: wild type vs cyclin mutants. 15 samples per time course at 16 min resolution. 2 biological replicates per strain.
2008-06-20 | E-GEOD-8799 | biostudies-arrayexpress
Project description:Cell cycle sensing of oxidative stress in Saccharomyces cerevisiae by oxidation of a specific cysteine residue in the transcription factor Swi6p. Yeast cells begin to bud and enter S phase when growth conditions are favourable during G1 phase. When subjected to oxidative stress, cells arrest at G1 delaying entry into the cell cycle allowing repair of cellular damage. Hence, oxidative stress sensing is coordinated with the regulation of cell cycle. We identified a redox sensing cysteine residue in the cell-cycle regulator of Saccharomyces cerevisiae, Swi6p, at position 404. Mutation of Cys404 to alanine abolished the ability of the cells to arrest at G1 upon treatment by lipid hydroperoxide. By constructing a truncated form of Swi6p, the Cys404 residue was found to be oxidised when cells were subjected to the oxidant. Furthermore, microarray analysis revealed that mutation of Cys404 to alanine led to loss of suppression of G1-cyclins CLN1 and PCL1 when the cells were exposed to lipid hydroperoxide. In conclusion, oxidation of Cys404 serves as a molecular sensor of oxidative stress and inhibits entry into the cell cycle by suppression of G1-cyclin expression.
2011-01-31 | GSE18334 | GEO
Project description:Cell cycle sensing of oxidative stress in Saccharomyces cerevisiae by oxidation of a specific cysteine residue in the transcription factor Swi6p. Yeast cells begin to bud and enter S phase when growth conditions are favourable during G1 phase. When subjected to oxidative stress, cells arrest at G1 delaying entry into the cell cycle allowing repair of cellular damage. Hence, oxidative stress sensing is coordinated with the regulation of cell cycle. We identified a redox sensing cysteine residue in the cell-cycle regulator of Saccharomyces cerevisiae, Swi6p, at position 404. Mutation of Cys404 to alanine abolished the ability of the cells to arrest at G1 upon treatment by lipid hydroperoxide. By constructing a truncated form of Swi6p, the Cys404 residue was found to be oxidised when cells were subjected to the oxidant. Furthermore, microarray analysis revealed that mutation of Cys404 to alanine led to loss of suppression of G1-cyclins CLN1 and PCL1 when the cells were exposed to lipid hydroperoxide. In conclusion, oxidation of Cys404 serves as a molecular sensor of oxidative stress and inhibits entry into the cell cycle by suppression of G1-cyclin expression. We used a gene expression approach to assess the involvement of Cys404 in oxidative stress by mutating this residue to alanine in order to study whether it contributes to Swi6p, a transcriptional factor, function for redox regulation of the cell cycle. Wild type, swi6-deletant, and swi6 C404A-mutated yeast cells were treated with either linoleic acid hydroperoxide (LoaOOH) or control. Three replicates per group/treatment.
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Project description:Distinct Signaling Roles of Ceramide Species in Yeast Revealed Through Integromics Analyses
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Project description:The large majority of oxidative lesions occurring in the G1 phase of the cell cycle are repaired by base excision repair (BER) rather than mismatch repair (MMR) to avoid long resections that can lead to genomic instability and cell death. However, how cells choose BER over MMR is not yet understood. Here, we show that, during G1, D-type cyclins are recruited to sites of oxidative DNA damage in a PCNA- and p21-dependent manner. In turn, in a manner that is independent on CDK4/6 activity, D-type cyclins stabilize p21, which competes through its PCNA-interacting protein (PIP) box with MMR components for their binding to PCNA. This reduces MMR activity while allowing BER. At the G1/S transition, the AMBRA1-dependent degradation of D-type cyclins renders p21 susceptible to proteolysis via SKP2 and CDT2. These timely degradation events allow the proper binding of MMR proteins to PCNA enabling the repair of DNA replication errors. Thus, the expression of D-type cyclins limit MMR in G1, whereas their degradation is necessary for proper MMR function in S. Defects in these two regulatory mechanisms promote genome instability. The mass spectrometry raw files correspond to the affinity purifications of proximity labeled (turbo-ID) PCNA and CCND1 under various conditions.
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