An essential role for the Ino80 chromatin remodeling complex in regulation of gene expression during cellular quiescence
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ABSTRACT:
PROVIDER: PRJNA824413 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18673711_1.fastq.gz | Fastqsanger.gz | |||
| SRR18673711_2.fastq.gz | Fastqsanger.gz | |||
| SRR18673712_1.fastq.gz | Fastqsanger.gz | |||
| SRR18673712_2.fastq.gz | Fastqsanger.gz | |||
| SRR18673713_1.fastq.gz | Fastqsanger.gz |
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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
Project description:During transcription, nucleosomes are evicted from regulatory and coding regions yet chromatin structure is stable. Restoration of chromatin structure involves concerted action of chromatin modifying activities. Our analysis demonstrates a genome wide function of the INO80 remodeling complex for stable repositioning of the nucleosome immediately proximal to the transcription initiation site. INO80 dependent remodeling of the promoter proximal nucleosomes has a global repressive role. Recruitment of INO80 to proximal nucleosomes overlaps with the elongating Polymerase II complex assembly. The amount of associated Polymerase II at start sites correlates with INO80 recruitment for inducible and constantly transcribed genes. Furthermore, at highly inducible promoters INO80 is required for repression of bidirectional transcription. Therefore, we suggest a function for INO80 after transcription initiation to achieve Polymerase II dependent reassembly of promoter proximal nucleosomes.
2016-12-24 | E-MTAB-1810 | biostudies-arrayexpress
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 the regulation of gene expression in G0 cells. We show that null mutants for two Ino80C subunits, Iec1 and Ies2, a putative subunit Arp42, a null mutant for the 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. Using spike in normalized ChIP-seq experiments, we show that there is a global reduction of H2A.Z levels in quiescent wild-type cells but not in iec1∆ cells and that a subtelomeric chromosome boundary element is strongly affected by Ino80C. Based on these observations, we propose a model in which Ino80C is evicting H2A.Z from chromatin in quiescent cells, thereby inactivating the subtelomeric boundary element, leading to a reorganization of the chromosome structure and activation of genes required to survive in quiescence.
| S-EPMC10097750 | biostudies-literature
Project description:Global regulation of H2A.Z localization by the INO80 chromatin remodeling enzyme is essential for genome integrity. Chromatin immunoprecipitation (ChIP) of Htz1 in wild-type and ino80 mutant yeast demonstrated that Ino80 plays a role in replacing Htz1 with H2A.
2010-12-01 | GSE25722 | GEO
Project description:Global regulation of H2A.Z localization by the INO80 chromatin remodeling enzyme is essential for genome integrity. Chromatin immunoprecipitation (ChIP) of Htz1 in wild-type and ino80 mutant yeast demonstrated that Ino80 plays a role in replacing Htz1 with H2A. Comparison of Htz1 localization in wt vs ino80 mutant yeast Prior to immunoprecipitation, cells arrested with alpha-factor or nocodazole: - The alpha-factor mating pheromone arrests yeast of the a mating type in the G1 phase of the cell cycle. - Nocodazole disrupts the polymerization of microtubules, blocking the cells from entering mitosis and arresting them in the G2/M phase of the cell cycle.
2010-12-01 | E-GEOD-25722 | biostudies-arrayexpress
Project description:INO80 is involved in many chromatin-dependent functions. However, its role in pluripotency has not been fully defined. We examined the impact of Ino80 deletion in the naïve and primed pluripotent stem cells. We found that Ino80 deletion had minimal effect on self-renewal and gene expression in the naïve state, but led to cellular differentiation and de-repression of developmental genes in the primed state. Mechanistically, INO80 co-occupied gene promoters that were bivalently marked by H3K4me3 and H3K27me3. Further, its occupancy was required for H3K27me3 installation and maintenance, as well as downstream gene repression. Finally, INO80 promoted H2A.Z occupancy at the bivalent domains, which in turn facilitated the polycomb repressive complex 2 (PRC2) recruitment. Together, our results identified the INO80-H2A.Z axis as an essential step for bivalent chromatin and poised gene expression and uncovered an epigenetic mechanism by which chromatin remodeling, histone variant, and histone modification coordinately control cell fate.
2021-07-04 | GSE158537 | GEO
Project description:INO80 is involved in many chromatin-dependent functions. However, its role in pluripotency has not been fully defined. We examined the impact of Ino80 deletion in the naïve and primed pluripotent stem cells. We found that Ino80 deletion had minimal effect on self-renewal and gene expression in the naïve state, but led to cellular differentiation and de-repression of developmental genes in the primed state. Mechanistically, INO80 co-occupied gene promoters that were bivalently marked by H3K4me3 and H3K27me3. Further, its occupancy was required for H3K27me3 installation and maintenance, as well as downstream gene repression. Finally, INO80 promoted H2A.Z occupancy at the bivalent domains, which in turn facilitated the polycomb repressive complex 2 (PRC2) recruitment. Together, our results identified the INO80-H2A.Z axis as an essential step for bivalent chromatin and poised gene expression and uncovered an epigenetic mechanism by which chromatin remodeling, histone variant, and histone modification coordinately control cell fate.
2021-07-04 | GSE158533 | GEO
Project description:INO80 is involved in many chromatin-dependent functions. However, its role in pluripotency has not been fully defined. We examined the impact of Ino80 deletion in the naïve and primed pluripotent stem cells. We found that Ino80 deletion had minimal effect on self-renewal and gene expression in the naïve state, but led to cellular differentiation and de-repression of developmental genes in the primed state. Mechanistically, INO80 co-occupied gene promoters that were bivalently marked by H3K4me3 and H3K27me3. Further, its occupancy was required for H3K27me3 installation and maintenance, as well as downstream gene repression. Finally, INO80 promoted H2A.Z occupancy at the bivalent domains, which in turn facilitated the polycomb repressive complex 2 (PRC2) recruitment. Together, our results identified the INO80-H2A.Z axis as an essential step for bivalent chromatin and poised gene expression and uncovered an epigenetic mechanism by which chromatin remodeling, histone variant, and histone modification coordinately control cell fate.
2021-07-04 | GSE158528 | GEO
Project description:INO80 is involved in many chromatin-dependent functions. However, its role in pluripotency has not been fully defined. We examined the impact of Ino80 deletion in the naïve and primed pluripotent stem cells. We found that Ino80 deletion had minimal effect on self-renewal and gene expression in the naïve state, but led to cellular differentiation and de-repression of developmental genes in the primed state. Mechanistically, INO80 co-occupied gene promoters that were bivalently marked by H3K4me3 and H3K27me3. Further, its occupancy was required for H3K27me3 installation and maintenance, as well as downstream gene repression. Finally, INO80 promoted H2A.Z occupancy at the bivalent domains, which in turn facilitated the polycomb repressive complex 2 (PRC2) recruitment. Together, our results identified the INO80-H2A.Z axis as an essential step for bivalent chromatin and poised gene expression and uncovered an epigenetic mechanism by which chromatin remodeling, histone variant, and histone modification coordinately control cell fate.
2021-07-04 | GSE158544 | GEO
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 | GSE116038 | GEO