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

ABSTRACT: 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.

ORGANISM(S): Schizosaccharomyces pombe

SUBMITTER: Kenichi Sajiki

PROVIDER: E-GEOD-14319 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

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

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

The putative ceramide-conjugation protein Cwh43 regulates G0 quiescence, nutrient metabolism and lipid homeostasis in fission yeast (Metabolome 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. Metabolome assay data is reported in the current study MTBLS577. Lipidome assay data associated to this study is reported in MTBLS578. Linked Studies: <a href='https://www.ebi.ac.uk/metabolights/MTBLS578' target='_blank'>MTBLS578</a>

2018-08-17 | MTBLS577 | MetaboLights

Leo1 is essential for dynamic regulation of heterochromatin and gene expression during cellular quiescence [RNA-Seq]

Project description:Cellular quiescence is a reversible differentiation state when cells are changing the gene expression programme to reduce metabolic functions and adapt to a new cellular environment. The epigenetic changes that accompany these alterations are not so well understood. Here we investigate the role of Leo1, a subunit of the conserved Paf1 (RNA polymerase-associated factor 1) complex, in the quiescence process using fission yeast as a model organism. Fission yeast cells enter the G0 phase of the cell cycle when exposed to nitrogen starvation and the heterochromatin regions become very dynamic. The reduction of heterochromatin in early G0 correlates with the reduced activity of target of rapamycin, TORC2, signalling. Cells lacking the Leo1 show reduced survival in G0. In these cells heterochromatin regions including subtelomeres are stabilized and many genes, including membrane transport genes, fail to be expressed. Our results suggest that Leo1 is essential for dynamic regulation of heterochromatin and gene expression during cellular quiescence.

2019-06-30 | GSE116657 | GEO

Leo1 is essential for dynamic regulation of heterochromatin and gene expression during cellular quiescence [ChIP microarray]

2019-06-30 | GSE116038 | GEO

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 ∆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.

2013-12-01 | GSE50986 | GEO

Distinctive responses to nitrogen starvation in the dominant active mutants of the fission yeast Rheb GTPase.

Project description:Rheb, a ras-like small GTPase conserved from human to yeast, controls Tor kinase and plays a central role in regulation of cell growth depending on extracellular conditions. Fission yeast Rheb regulates amino acid uptake as well as response to nitrogen starvation. In this study we generated two mutants of Rheb, rhb1-DA4 and rhb1-DA8, and characterized them genetically. V17A mutation within the G1 box defined for the ras-like GTPases was responsible for rhb1-DA4, and Q52R I76F within the switch II domain for rhb1-DA8. In fission yeast, two events, induction of a meiosis initiating gene mei2+ and cell division without cell growth, are a typical response to nitrogen starvation. Under nitrogen-rich conditions, Rheb stimulates Tor kinase, which, in turn, suppresses the response to nitrogen starvation. While amino acid uptake was prevented by both rhb1-DA4 and rhb1-DA8 in a dominant fashion, the response to nitrogen starvation was prevented only by rhb1-DA4. rhb1-DA8 thereby allowed genetic dissection of the Rheb-dependent signaling cascade. We postulate that Rheb in fission may have two downstream elements, Tor kinase for regulation of the response to nitrogen starvation and the other element for regulation of amino acid uptake. Gene expression profile under nitrogen starvation in fission yeast. Type of experiment: Comparing between vegetatively-growing control cells and cells 3 hrs after nitrogen starvation. Experimental factor: Gene expression profile after nitrogen starvation in the rhb1-D4 or rhb1-D8 cells. Quality control steps taken: All experiments were repeated more than twice except for the tsc2D which was previously reported. Keywards: Nitrogen starvation, rhb1-D4, rhb1-D8

2009-09-28 | E-GEOD-14626 | biostudies-arrayexpress

CROP: A Retromer- PROPPIN complex mediating membrane fission in the endo-lysosomal system

Project description:Endo-lysosomal compartments exchange proteins by fusing, fissioning, and through endosomal transport carriers. Thereby, they sort many plasma membrane receptors and transporters and control cellular signaling and metabolism. How the membrane fission events are catalyzed is poorly understood. Here, we identify the novel CROP complex as a factor acting at this step. CROP integrates PROPPIN Atg18 with a part of the endosome- and vacuole-associated retromer complex to generate a membrane fission device of much higher potency. We studied its activity in yeast, in human cells and on liposomes.

2022-05-05 | PXD031244 | Pride

MetaboLights MTBLS577 - GNPS The putative ceramide-conjugation protein Cwh43 regulates G0 quiescence, nutrient metabolism and lipid homeostasis in fission yeast (Metabolome 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. Metabolome assay data is reported in the current study MTBLS577. Lipidome assay data associated to this study is reported in MTBLS578. Linked Studies: <a href='https://www.ebi.ac.uk/metabolights/MTBLS578' target='_blank'>MTBLS578</a>

2020-07-20 | MSV000085791 | GNPS

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