Refined mechanism of promoter Nucleosome-Depleted Regions resetting after replication
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ABSTRACT:
PROVIDER: PRJNA1090510 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28411500_1.fastq.gz | Fastqsanger.gz | |||
| SRR28411500_2.fastq.gz | Fastqsanger.gz | |||
| SRR28411501_1.fastq.gz | Fastqsanger.gz | |||
| SRR28411501_2.fastq.gz | Fastqsanger.gz | |||
| SRR28411502_1.fastq.gz | Fastqsanger.gz |
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Project description:Replication disrupts chromatin organization. Thus, rapid resetting of nucleosome positioning is essential to maintain faithful gene expression. The initial step of this reconfiguration occurs at Nucleosome-Depleted Regions (NDRs). While studies have elucidated the role of Transcription Factors (TFs) and Chromatin Remodelers (CRs) in vitro or in maintaining NDRs in vivo, none has addressed their in vivo function shortly after replication. Through purification of nascent chromatin coupled with yeast genetics, we dissected the choreography of events governing the proper positioning of the -1/+1 nucleosomes flanking promoter NDRs. Our findings reveal that CRs are the primary contributors of -1/+1 repositioning post-replication, with RSC acting upstream of INO80. Surprisingly, while Reb1 and Abf1 TFs are not essential for NDR resetting, they are required for NDR maintenance via the promotion of H3 acetylations. Taken together, we propose a two-step model for NDR resetting in S. cerevisiae: first, CRs alone reset promoter NDRs after replication, while a combination of TFs and CRs is required for subsequent maintenance.
2024-03-25 | GSE262171 | GEO
Project description:Previous studies indicate that eukaryotic promoters display a stereotypical chromatin landscape characterized by a well-positioned +1 nucleosome near the transcription start site and an upstream -1 nucleosome that together demarcate a nucleosome-free (or depleted) region. Here we present evidence that there are two distinct types of promoters distinguished by the resistance of the -1 nucleosome to micrococcal nuclease digestion. These different architectures are characterized by two sequence motifs that are broadly deployed at one set of promoters where a nuclease-sensitive ("fragile") nucleosome forms, but concentrated in a more narrow, nucleosome-free region at all other promoters. The RSC nucleosome remodeler acts through the motifs to establish stable +1 and -1 nucleosome positions, while binding of a small set of general regulatory (pioneer) factors at fragile nucleosome promoters plays a key role in their destabilization. We propose that the fragile nucleosome promoter architecture is adapted for regulation of highly expressed, growth-related genes. MNase-seq profiles obtained with various MNase concentrations from wild-type cells and cells depleted of different factors. ChIP-seq using anti-RNA polymerase II antibody, anti-histone H2A antibody, and anti-histone H3 antibody.
2015-11-05 | E-GEOD-73337 | biostudies-arrayexpress
Project description:Nucleosome positioning in the genome is essential for the regulation of many nuclear processes. We currently have limited capability to predict nucleosome positioning in vivo, especially the locations and sizes of nucleosome depleted regions (NDRs). Here, we present a thermodynamic model that incorporates the intrinsic affinity of histones, competitive binding of sequence-specific factors, and nucleosome remodeling to predict nucleosome positioning in budding yeast. The model shows that the intrinsic affinity of histones, at near-saturating histone concentration, is not sufficient in generating NDRs in the genome. However, the binding of a few factors, especially RSC towards GC-rich and poly(A/T) sequences, allows us to predict ~ 66% of genome-wide NDRs. The model also shows that nucleosome remodeling activity is required to predict the correct NDR sizes. The validity of the model was further supported by the agreement between the predicted and the measured nucleosome positioning upon factor deletion or on exogenous sequences introduced into yeast. Overall, our model quantitatively evaluated the impact of different genetic components on NDR formation and illustrated the vital roles of sequence-specific factors and nucleosome remodeling in this process.
| S-EPMC7822557 | biostudies-literature
Project description:The occupancy of nucleosomes governs access to the eukaryotic genomes and results from a combination of biophysical features and the effect of ATP-dependent remodeling complexes. Most promoter regions show a conserved pattern characterized by a nucleosome-depleted region (NDR) flanked by nucleosomal arrays. The conserved RSC remodeler was reported to be critical to establish NDR in vivo in budding yeast but other evidences suggested that this activity may not be conserved in fission yeast. By reanalysing and expanding previously published data, we propose that NDR formation is dependent on RSC in both yeast species. We also discuss the most prominent biological role of RSC and the possibility that non-essential subunits define alternate versions of the complex.
2016-08-24 | GSE84912 | GEO
Project description:The chromatin architecture of eukaryotic gene promoters is generally characterized by a nucleosome-free region (NFR) flanked by at least one H2A.Z variant nucleosome. Computational predictions of nucleosome positions based on thermodynamic properties of DNA-histone interactions have met with limited success. Here we show that the action of the essential RSC remodeling complex in S. cerevisiae helps explain the discrepancy between theory and experiment. In RSC-depleted cells, NFRs shrink such that the average positions of flanking nucleosomes move toward predicted sites. Nucleosome positioning at distinct subsets of promoters additionally requires the essential Myb family proteins Abf1 and Reb1, whose binding sites are enriched in NFRs. In contrast, H2A.Z deposition is dispensable for nucleosome positioning. By regulating H2A.Z deposition using a steroid-inducible protein splicing strategy, we show that NFR establishment is necessary for H2A.Z deposition. These studies suggest an ordered pathway for the assembly of promoter chromatin architecture.
2009-05-01 | GSE13446 | GEO
Project description:DNA Methylation-Based High-Resolution Mapping of Long-Distance Chromosomal Interactions in Nucleosome-Depleted Regions
| PRJNA1013317 | ENA
Project description:The occupancy of nucleosomes governs access to the eukaryotic genomes and results from a combination of biophysical features and the effect of ATP-dependent remodeling complexes. Most promoter regions show a conserved pattern characterized by a nucleosome-depleted region (NDR) flanked by nucleosomal arrays. The conserved RSC remodeler was reported to be critical to establish NDR in vivo in budding yeast but other evidences suggested that this activity may not be conserved in fission yeast. By reanalysing and expanding previously published data, we propose that NDR formation is dependent on RSC in both yeast species. We also discuss the most prominent biological role of RSC and the possibility that non-essential subunits define alternate versions of the complex. Samples from mononucleosomal DNA from S. pombe strains h- kanR-tetO-snf21-Tap-natR ura4::rTetR-tup11 were sequenced (Illumina NextSeq 500 platform) using the pair-end read protocol
2016-08-24 | E-GEOD-84912 | biostudies-arrayexpress
Project description:Previous studies indicate that eukaryotic promoters display a stereotypical chromatin landscape characterized by a well-positioned +1 nucleosome near the transcription start site and an upstream -1 nucleosome that together demarcate a nucleosome-free (or depleted) region. Here we present evidence that there are two distinct types of promoters distinguished by the resistance of the -1 nucleosome to micrococcal nuclease digestion. These different architectures are characterized by two sequence motifs that are broadly deployed at one set of promoters where a nuclease-sensitive ("fragile") nucleosome forms, but concentrated in a more narrow, nucleosome-free region at all other promoters. The RSC nucleosome remodeler acts through the motifs to establish stable +1 and -1 nucleosome positions, while binding of a small set of general regulatory (pioneer) factors at fragile nucleosome promoters plays a key role in their destabilization. We propose that the fragile nucleosome promoter architecture is adapted for regulation of highly expressed, growth-related genes.
2015-11-05 | GSE73337 | GEO
Project description:Nucleosome-depleted regions (NDRs) are ubiquitous on eukaryotic promoters. The formation of many NDRs cannot be readily explained by previously proposed mechanisms. Here, we carry out a focused study on a physiologically important NDR in the yeast CLN2 promoter (CLN2pr). We show that this NDR does not result from intrinsically unfavorable histone-DNA interaction. Instead, we identified eight conserved factor binding sites, including that of Reb1, Mcm1, and Rsc3, that cause the local nucleosome depletion. These nucleosome-depleting factors (NDFs) work redundantly, and simultaneously mutating all their binding sites eliminates CLN2pr NDR. The loss of the NDR induces unreliable "on/off" expression in individual cell cycles, but in the presence of the NDR, NDFs have little direct effect on transcription. We present bioinformatic evidence that the formation of many NDRs across the genome involves multiple NDFs. Our findings also provide significant insight into the composition and spatial organization of functional promoters.
| S-EPMC3119483 | biostudies-literature
Project description:The chromatin architecture of eukaryotic gene promoters is generally characterized by a nucleosome-free region (NFR) flanked by at least one H2A.Z variant nucleosome. Computational predictions of nucleosome positions based on thermodynamic properties of DNA-histone interactions have met with limited success. Here we show that the action of the essential RSC remodeling complex in S. cerevisiae helps explain the discrepancy between theory and experiment. In RSC-depleted cells, NFRs shrink such that the average positions of flanking nucleosomes move toward predicted sites. Nucleosome positioning at distinct subsets of promoters additionally requires the essential Myb family proteins Abf1 and Reb1, whose binding sites are enriched in NFRs. In contrast, H2A.Z deposition is dispensable for nucleosome positioning. By regulating H2A.Z deposition using a steroid-inducible protein splicing strategy, we show that NFR establishment is necessary for H2A.Z deposition. These studies suggest an ordered pathway for the assembly of promoter chromatin architecture. Nucleosome positions were mapped in a variety of strains under a variety of conditions to determine how several proteins are involved in nucleosome positioning. All replicates are biological replicates. Each set of replicates is balanced in terms of Cy3:Cy5 such that there are equal numbers of Cy3:Cy5 and Cy5:Cy3 arrays (format: mononucleosomal DNA:reference DNA). Changes in gene expression in a strain carrying either the Sth1-degron or Abf1-Reb1-degron under degron-inducing conditions were profiled by hybridizing labeled cDNA derived from the degron strain against labeled cDNA derived from a control strain lacking the degron, but grown under the same conditions. Four biological replicates for each experiment were done using a balanced dye-swap design.
2009-04-30 | E-GEOD-13446 | biostudies-arrayexpress