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Ccr4-Not complex reduces transcription efficiency in heterochromatin

ABSTRACT: Ccr4-Not complex reduces transcription efficiency in heterochromatin

PROVIDER: PRJNA773101 | ENA |

REPOSITORIES: ENA

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Ccr4-Not complex reduces transcription efficiency in heterochromatin

Project description:Heterochromatic silencing is thought to occur through a combination of transcriptional silencing and RNA degradation, but the relative contribution of each pathway is not known. In this study we analyzed RNA Polymerase II (RNA Pol II) occupancy and levels of nascent and steady-state RNA in different strains of fission yeast, in order to quantify the contribution of each pathway to heterochromatic silencing. We found that transcriptional silencing consists of two components, reduced RNA Pol II accessibility and, unexpectedly, reduced transcriptional efficiency. Heterochromatic loci showed lower transcriptional output compared to euchromatic loci, despite the presence of comparable amounts of RNA Pol II in both types of regions. We determined that the Ccr4-Not complex and H3K9 methylation are required for reduced transcriptional efficiency in heterochromatin and that a subset of heterochromatic RNA is degraded more rapidly than euchromatic RNA. Finally, we quantified the contribution of different chromatin modifiers, RNAi and RNA degradation to each silencing pathway. Our data show that several pathways contribute to heterochromatic silencing in a locus-specific manner and reveal transcriptional efficiency as a new mechanism of silencing.

2022-06-15 | GSE186273 | GEO

Role of the Ccr4/Not complex in the regulation of heterochromatin in Schizosaccharomyces pombe

Project description:ChIP-seq experiments to investigate heterochromatin structure in wild type, caf1, ccr4 and mmi1 mutants of fission yeast

2015-09-28 | E-MTAB-3036 | biostudies-arrayexpress

Role of Ccr4-Not Complex in Heterochromatin Formation at Meiotic Genes and Subtelomeres in Fission Yeast (VII)

Project description:ChIP-seq experiments to investigate heterochromatin structure in wild type, ccr4, not2 and not4 mutants of fission yeast

2015-09-28 | E-MTAB-3490 | biostudies-arrayexpress

Role of the Ccr4/Not complex in the regulation of heterochromatin in Schizosaccharomyces pombe (IV)

Project description:Expression profiling of mutants of genes encoding components of the Ccr4-Not complex and other related genes

2015-09-25 | E-MTAB-3059 | biostudies-arrayexpress

Role of the Ccr4/Not complex in the regulation of heterochromatin in Schizosaccharomyces pombe (V)

Project description:Expression profiling of mutants of genes encoding components of the Ccr4-Not complex and other related genes

2015-09-25 | E-MTAB-3060 | biostudies-arrayexpress

Role of the Ccr4/Not complex in the regulation of heterochromatin in Schizosaccharomyces pombe (II)

Project description:RIP-chip experiments to identify RNAs associated with components of the Ccr4-Not complex in fission yeast

2015-09-25 | E-MTAB-3057 | biostudies-arrayexpress

Role of the Ccr4/Not complex in the regulation of heterochromatin in Schizosaccharomyces pombe (VI)

Project description:RIP-chip experiments to identify RNAs associated with components of the Ccr4-Not complex in fission yeast

2015-09-25 | E-MTAB-3065 | biostudies-arrayexpress

The Ccr4-Not complex regulates TORC1 signaling and mitochondrial metabolism by promoting vacuole V-ATPase activity

Project description:The Ccr4-Not complex is an effector of multiple signaling pathways controlling gene transcription and mRNA turnover. Herein, we provide evidence that Ccr4-Not also activates nutrient signaling through the essential target of rapamycin complex 1 (TORC1) pathway. Mechanistically, Ccr4-Not loss decreases TORC1 signaling due to reduced stability of the vacuole V-ATPase that is required to activate TORC1 when associated with the Gtr1 GTPase containing EGO complex. Expressing a constitutively active Gtr1 in Ccr4-Not deficient cells bypasses the requirement for the V-ATPase and restores TORC1 signaling. Transcriptome analysis reveals that Ccr4-Not loss activates TORC1 repressed retrograde signaling to remodel metabolism and enhance mitochondrial function. Blocking retrograde signaling in a Ccr4-Not mutant further reduces TORC1 signaling, thus suggesting the enhanced mitochondrial metabolism due to Ccr4-Not loss is a metabolic adaptive response required to sustain TORC1 activity. Therefore, Ccr4-Not is a critical activator of TORC1 signaling that regulates cellular metabolism.

2019-10-04 | GSE138363 | GEO

The CCR4-NOT Complex Is Implicated in the Viability of Aneuploid Yeasts

Project description:To identify the genes required to sustain aneuploid viability, we screened a deletion library of non-essential genes in the fission yeast Schizosaccharomyces pombe, in which most types of aneuploidy are eventually lethal to the cell. Aneuploids remain viable for a period time and can form colonies by reducing the extent of the aneuploidy. We hypothesized that a reduction in colony formation efficiency could be used to screen for gene deletions that compromise aneuploid viability. Deletion mutants were used to measure the effects on the viability of spores derived from triploid meiosis and from a chromosome instability mutant. We found that the CCR4-NOT complex, an evolutionarily conserved general regulator of mRNA turnover, and other related factors, including poly(A)-specific nuclease for mRNA decay, are involved in aneuploid viability. Defective mutations in CCR4-NOT complex components in the distantly related yeast Saccharomyces cerevisiae also affected the viability of spores produced from triploid cells, suggesting that this complex has a conserved role in aneuploids. In addition, our findings suggest that the genes required for homologous recombination repair are important for aneuploid viability. Gene expression profile at exponentially-growing phase.in the fission yeast deletion mutants of the CCR4-NOT complex protein genes.

2012-06-26 | E-GEOD-36454 | biostudies-arrayexpress

The CCR4-NOT complex suppresses untimely translational activation of maternal mRNAs.

Project description:Control of mRNA poly(A) tail has central role to regulate mRNA metabolism: translation efficiency and mRNA stability. Gene expression in maturing oocytes largely relies on the regulation of mRNA metabolism as they are transcriptionally silent. The CCR4-NOT complex is a major deadenylase for mammals and regulates poly(A) tails of maternal mRNAs, however their function to translational regulation was not well understood. Here we show that CCR4-NOT suppresses translational activity of maternal mRNAs during oocyte maturation. Oocytes which lack entire deadenylase activity of CCR4-NOT by genetic deletion of its catalytic subunits: CNOT7 and CNOT8 showed increase of both expression of maternal mRNAs and translational activity of them during oocyte maturation.

2023-10-01 | GSE224308 | GEO

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