Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from fission yeast deletion mutant of Klf1, a C2H2 zinc finger-transcription factor, in G0 and VE phases

ABSTRACT: Fission yeast Schizosaccharomyces pombe is a model for studying cellular quiescence. Shifting to medium without a nitrogen-source induces proliferative cells to enter long-term G0 quiescence. Klf1 is a Kruppel-like transcription factor with a 7-amino acid-spaced C2H2-type zinc finger motif. The deletion mutant ∆klf1 normally divides in vegetative medium, but proliferation is not restored after long-term G0 quiescence. Cell biologic, transcriptomic, and metabolomic analyses revealed a unique phenotype of the ∆klf1 mutant in quiescence. Mutant cells had diminished transcripts related to signaling molecules for switching to differentiation. In contrast, proliferative metabolites for cell-wall assembly and antioxidants significantly increased. Further, the size of the ∆klf1 cells is markedly increased during quiescence due to the aberrant accumulation of calcofluor-positive chitin-like materials beneath the cell wall. After 4 weeks quiescence, the ability for reversible proliferation is lost, but energy metabolism is maintained. Klf1 thus plays a role in G0 phase longevity through enhancing the differentiation signal and suppressing metabolism for growth. If Klf1 is lost, S. pombe fails to maintain a constant cell size during quiescence.

ORGANISM(S): Saccharomyces cerevisiae Schizosaccharomyces pombe

PROVIDER: GSE50986 | GEO | 2013/12/01

SECONDARY ACCESSION(S): PRJNA219487

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from fission yeast deletion mutant of Klf1, a C2H2 zinc finger-transcription factor, in G0 and VE phases

Project description:Fission yeast Schizosaccharomyces pombe is a model for studying cellular quiescence. Shifting to medium without a nitrogen-source induces proliferative cells to enter long-term G0 quiescence. Klf1 is a Kruppel-like transcription factor with a 7-amino acid-spaced C2H2-type zinc finger motif. The deletion mutant M-bM-^HM-^Fklf1 normally divides in vegetative medium, but proliferation is not restored after long-term G0 quiescence. Cell biologic, transcriptomic, and metabolomic analyses revealed a unique phenotype of the M-bM-^HM-^Fklf1 mutant in quiescence. Mutant cells had diminished transcripts related to signaling molecules for switching to differentiation. In contrast, proliferative metabolites for cell-wall assembly and antioxidants significantly increased. Further, the size of the M-bM-^HM-^Fklf1 cells is markedly increased during quiescence due to the aberrant accumulation of calcofluor-positive chitin-like materials beneath the cell wall. After 4 weeks quiescence, the ability for reversible proliferation is lost, but energy metabolism is maintained. Klf1 thus plays a role in G0 phase longevity through enhancing the differentiation signal and suppressing metabolism for growth. If Klf1 is lost, S. pombe fails to maintain a constant cell size during quiescence. Gene expression profile of fission yeast wild type cells and klf1-gene disruptant cells in proliferating state and in quiescent state. Type of experiment: Comparing between wild type cells and klf1-gene disruptant cells in proliferating condition and in quiescent condition. Experimental factor: Exponentially proliferating state in synthetic medium, EMM2, and quiescent G0 state in nitrogen-depleted synthetic medium, EMM2-N. Quality control steps taken: All experiments were repeated twice in each condition.

2013-12-01 | E-GEOD-50986 | biostudies-arrayexpress

Whole-cell proteome analyses of prototrophic Schizosaccharomyces pombe wild-type and mug174Δ strains during vegetative growth and in G0/cellular quiescence (1 day, 7 days, or 14 days following nitrogen depletion) using liquid chromatography followed by tandem mass spectrometry (LC-MS/MS) and the label-free quantitative proteomics method.

Project description:Using a whole-cell proteome approach, we investigated the effect of the mug174+ gene deletion on the proteome during vegetative growth and G0/cellular quiescence in the fission yeast Schizosaccahromyces pombe. We revealed that (1) Mug174 ensured the protein expression from intron-containing genes during vegetative growth, and (2) the proteins involved in ribosome biogenesis were increased, whereas some of the G0 essential proteins were decreased in the absence of Mug174. The data from our proteome analyses indicated that Mug174 is essential for proper protein expression.

2024-10-17 | PXD052066 | Pride

A screen for histone mutations that affect quiescence in S. cerevisiae.

Project description:Quiescence is a distinct cell cycle phase, termed G0, in which growth, transcription, translation, and replication are suppressed. Yeast cells enter G0 following glucose exhaustion but remain viable for an extended period and can re-enter the cell cycle when returned to glucose-rich medium. Quiescence is a feature of all organisms and is essential for the maintenance of stem cells and tissue renewal. Quiescence is also related to chronological lifespan (CLS) - or the capacity of post-mitotic quiescent cells to survive over time - and thus contributes to longevity. However, important questions remain to be answered regarding the mechanisms that control entry into quiescence, the maintenance of quiescence, and the re-entry of quiescent cells into the cell cycle. Histone acetylation is lost during the formation of quiescent yeast cells, and chromatin becomes highly condensed. This unique chromatin landscape plays a key role in supporting quiescence-specific transcriptional repression and has been linked to the formation and maintenance of quiescent cells. To ask if other chromatin features regulate quiescence, we conducted a comprehensive screen of histone H3 and H4 mutants. We identified several mutants that show altered quiescence entry and have characterized their chromatin phenotypes. None of these mutants retain histone acetylation, while several have altered chromatin condensation. Additionally, a screen for H3 and H4 mutants with altered chronological lifespan showed that CLS is highly correlated with quiescence entry.

2023-03-01 | GSE210305 | GEO

Specific biomarkers for stochastic division patterns and starvation-induced quiescence under limited glucose levels in fission yeast

Project description:Glucose as a source of energy is centrally important to our understanding of life. We investigated the cell division-quiescence behavior of the fission yeast Schizosaccharomyces pombe under a wide range of glucose concentrations (0-111 mM). The mode of S. pombe cell division under a microfluidic perfusion system was surprisingly normal under highly diluted glucose concentrations (5.6 mM, 1/20 of the standard medium, within human blood sugar levels). Division became stochastic, accompanied by a curious division-timing inheritance, in 2.2-4.4 mM glucose. A critical transition from division to quiescence occurred within a narrow range of concentrations (2.2-1.7 mM). Under starvation (1.1 mM) conditions, cells were mostly quiescent and only a small population of cells divided. Under fasting (0 mM) conditions, division was immediately arrested with a short chronological lifespan (16 h). When cells were first glucose starved prior to fasting, they possessed a substantially extended lifespan (∼14 days). We employed a quantitative metabolomic approach for S. pombe cell extracts, and identified specific metabolites (e.g. biotin, trehalose, ergothioneine, S-adenosyl methionine and CDP-choline), which increased or decreased at different glucose concentrations, whereas nucleotide triphosphates, such as ATP, maintained high concentrations even under starvation. Under starvation, the level of S-adenosyl methionine increased sharply, accompanied by an increase in methylated amino acids and nucleotides. Under fasting, cells rapidly lost antioxidant and energy compounds, such as glutathione and ATP, but, in fasting cells after starvation, these and other metabolites ensuring longevity remained abundant. Glucose-starved cells became resistant to 40 mM H(2)O(2) as a result of the accumulation of antioxidant compounds.

2017-07-06 | MTBLS316 | MetaboLights

Cellular quiescence is dependent upon the HIRA histone chaperone

Project description:Quiescence (G0) is a reversible non-dividing state that facilitates cellular survival in adverse conditions. Here we demonstrate that the function of the HIRA histone chaperone complex is required for viability during nitrogen-starvation induced quiescence in Schizosaccharomyces pombe. G0 cells lacking the HIRA protein, Hip1 exhibit elevated levels of antisense ncRNAs and an increase in unrepaired DNA double strand breaks. Nitrogen-starved hip1∆ cells retain metabolic activity but, in contrast to wild type, rapidly lose the ability to resume proliferation. After a short period in G0 (1 day), hip1∆ mutants are able to resume cell growth in response to the restoration of a nitrogen source, but do not efficiently induce Start-specific gene expression and re-enter the cell cycle. However, hip1∆ cells rapidly progress to an unresponsive state and by 4 days in G0, the majority no longer initiate growth following nitrogen source restoration. Analysis using a conditional hip1 allele is consistent with these findings and indicates that HIRA is required for efficient exit from quiescence and prevents a permanent cell cycle arrest.

2023-11-13 | GSE129599 | GEO

Novel roles of small extracellular vesicles in regulating the quiescence and proliferation of neural stem cells

Project description:We analyzed protein cargos of NSC sEVs from proliferating, resting and reactivating status by proteomics approaches. Our results revealed specific functional clusters of pathways in gene ontology annotations of differentially expressed proteins in three sources of exosomes. Furthermore, we showed the involvement of sEVs in maintaining quiescence, along with entering and exiting the G0 phase by applying an exosome inhibitor. Our findings highlighted the expression level changes of NSCs of sEV protein cargo at different proliferative conditions and further confirmed the involvement of sEVs in entering, maintaining and exiting quiescence of NSCs.

2021-10-27 | PXD027651 | JPOST Repository

Transcription profiling of S. pombe to investigate genetic control of cellular quiescence

Project description:Transition from proliferation to quiescence brings about extensive changes in cellular behavior and structure. However, genes critical for establishing and/or for maintaining quiescence are largely unknown. The fission yeast S. pombe is found as an excellent model for studying this problem, because it becomes quiescent under nitrogen starvation. Here we characterize 610 temperature-sensitive (ts) mutants, and identify 33 genes required for entry into and the maintenance of quiescence. These genes cover a broad range of cellular functions in the cytoplasm, membrane and the nucleus, encoding proteins for stress-responsive and cell cycle kinase signaling pathway, actin-bound and osmo-controlling endosome formation, RNA transcription, splicing and ribosome biogenesis, chromatin silencing, biosynthesis of lipid and ATP, cell wall and membrane morphogenesis, protein trafficking and vesicle fusion. We specifically highlight Fcp1, CTD phosphatase of RNA polymerase II, which differentially affects transcription of genes involved in quiescence and proliferation. We propose that the transcriptional role of Fcp1 is central to differentiate quiescence from proliferation. Experiment Overall Design: Gene expression profile under nitrogen rich or starved condition at 26ÂºC or 37ÂºC in WT (L972) or fcp1-452 ts mutant strain of fission yeast.

2009-05-11 | E-GEOD-14319 | biostudies-arrayexpress

An essential role for the Ino80 chromatin remodeling complex in regulation of gene expression during cellular quiescence

Project description:Cellular quiescence is an important physiological state both in unicellular and multicellular eukaryotes. Quiescent cells are halted for proliferation and stop the cell cycle at the G0 stage. Using fission yeast as a model organism, we have previously found that several subunits of a conserved chromatin remodeling complex, Ino80C (INOsitol requiring nucleosome remodeling factor), are required for survival in quiescence. Here, we demonstrate that Ino80C has a key function in regulation of gene expression in G0 cells. We show that null mutants for two Ino80C subunits Arp42 and Iec1, a null mutant for histone variant H2A.Z, and a null mutant for the Inositol kinase Asp1 have very similar phenotypes in quiescence. These mutants show reduced transcription genome-wide, and specifically fail to activate 149 quiescence genes, of which many are localized to the subtelomeric regions. Based on these observations and previous findings, we propose a model in which Ino80C, modulated by Inositol kinase activity, is required to remove H2A.Z, especially in subtelomeric regions in order to reorganize the chromosome structure and activate genes required to survive in quiescence.

2023-04-19 | GSE200378 | GEO

Genetic Control of Cellular Quiescence in S. pombe

Project description:Transition from proliferation to quiescence brings about extensive changes in cellular behavior and structure. However, genes critical for establishing and/or for maintaining quiescence are largely unknown. The fission yeast S. pombe is found as an excellent model for studying this problem, because it becomes quiescent under nitrogen starvation. Here we characterize 610 temperature-sensitive (ts) mutants, and identify 33 genes required for entry into and the maintenance of quiescence. These genes cover a broad range of cellular functions in the cytoplasm, membrane and the nucleus, encoding proteins for stress-responsive and cell cycle kinase signaling pathway, actin-bound and osmo-controlling endosome formation, RNA transcription, splicing and ribosome biogenesis, chromatin silencing, biosynthesis of lipid and ATP, cell wall and membrane morphogenesis, protein trafficking and vesicle fusion. We specifically highlight Fcp1, CTD phosphatase of RNA polymerase II, which differentially affects transcription of genes involved in quiescence and proliferation. We propose that the transcriptional role of Fcp1 is central to differentiate quiescence from proliferation. Keywords: cell cycle control, protein trafficking, cortex actin, RNA polymerase II, protein phosphatase

2009-04-30 | GSE14319 | GEO

The putative ceramide-conjugation protein Cwh43 regulates G0 quiescence, nutrient metabolism and lipid homeostasis in fission yeast (Lipidome assay)

Project description:Cellular nutrient states control whether cells proliferate, or whether they enter or exit quiescence. Here, we report characterizations of fission yeast temperature-sensitive (ts) mutants of the evolutionarily conserved transmembrane protein, Cwh43, and explore its relevance to utilization of glucose, nitrogen-source, and lipids. GFP-tagged Cwh43 localizes at ER associated with the nuclear envelope and the plasma membrane, as in budding yeast. We found that cwh43 mutants failed to divide in low glucose and lost viability during quiescence under nitrogen starvation. In cwh43 mutant, comprehensive metabolome analysis demonstrated dramatic changes in marker metabolites that altered under low glucose and/or nitrogen starvation, although cwh43 apparently consumed glucose in the culture media. Furthermore, we found that cwh43 mutant had elevated levels of triacylglycerols (TGs) and coenzyme A, and that it accumulated lipid droplets. Notably, TG biosynthesis was required to maintain cell division in cwh43 mutant. Thus, Cwh43 affects utilization of glucose and nitrogen-sources, as well as storage lipid metabolism. These results may fit to a notion developed in budding yeast that Cwh43 conjugates ceramide to GPI (glycosylphosphatidylinositol)-anchored proteins and maintains integrity of membrane organization. Lipidome assay data is reported in the current study MTBLS578. Metabolome assay data associated to this study is reported in MTBLS577. Linked Studies: <a href='https://www.ebi.ac.uk/metabolights/MTBLS577' target='_blank'>MTBLS577</a>

2018-08-21 | MTBLS578 | MetaboLights

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data