Saccharomyces cerevisiae
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ABSTRACT:
PROVIDER: PRJNA102223 | ENA |
REPOSITORIES: ENA
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Project description:Nucleosomes restrict the access of transcription factors to chromatin. RSC is a SWI/SNF-family chromatin-remodeling complex from yeast that repositions and ejects nucleosomes in vitro. Here, we examined these activities and their importance in vivo. We utilized array-based methods to examine nucleosome occupancy and positioning at more than 200 locations in the genome following the controlled destruction of the catalytic subunit of RSC, Sth1. Loss of RSC function caused pronounced and general reductions in transcription from Pol I, II, and III genes. At Pol III genes, Sth1 loss conferred a general gain in nucleosome density and an accompanying reduction in RNA Pol III occupancy. In contrast, we observed primarily single nucleosome changes, including movement, at Pol II promoters. Importantly, a greater number of changes were observed near the transcription start sites of RSC-occupied promoters than non-occupied promoters. These changes are distinct from those due to general loss of transcription. Thus, RSC action affects both nucleosome density and positioning in vivo, but applies these remodeling modes differently at Pol II and Pol III genes. Keywords: ChIP-chip, nucleosome, mononucleosome, RSC, transcription
2007-12-01 | GSE8862 | GEO
Project description:Mammalian nuclei contain Pol I, Pol II, and Pol III. However, to what extent and how they are cross-regulated remains elusive. Here, we performed orthogonal multi-omics profiling after acute degradation of the largest subunits of Pol I, Pol II, and Pol III, and showed that they mainly affect specific genes. In contrast, the loss of Pol I or Pol II causes few changes for other RNA polymerases and confirms those known. The changes of Pol II transcription after Pol III depletion are the largest among all the cross-regulatory types. Meta-analyses reveal that Pol III depletion increases nucleosome positioning, reduces the FACT complex occupancy, and perturbs Pol II elongation for nearby mRNA genes. Furthermore, the nucleosome positioning changes also underpinning the Pol II effects on Pol III-mediated tRNA transcription. Our results suggest that Pol III works together with Pol II to coordinate their transcription activities by maintaining local chromatin architecture.
2022-11-07 | GSE217478 | GEO
Project description:Mammalian nuclei contain Pol I, Pol II, and Pol III. However, to what extent and how they are cross-regulated remains elusive. Here, we performed orthogonal multi-omics profiling after acute degradation of the largest subunits of Pol I, Pol II, and Pol III, and showed that they mainly affect specific genes. In contrast, the loss of Pol I or Pol II causes few changes for other RNA polymerases and confirms those known. The changes of Pol II transcription after Pol III depletion are the largest among all the cross-regulatory types. Meta-analyses reveal that Pol III depletion increases nucleosome positioning, reduces the FACT complex occupancy, and perturbs Pol II elongation for nearby mRNA genes. Furthermore, the nucleosome positioning changes also underpinning the Pol II effects on Pol III-mediated tRNA transcription. Our results suggest that Pol III works together with Pol II to coordinate their transcription activities by maintaining local chromatin architecture.
2022-11-07 | GSE217477 | GEO
Project description:Genome binding/occupancy profiling by high throughput sequencing ｜ Expression profiling by high throughput sequencing | Other Mammalian nuclei contain Pol I, Pol II, and Pol III. However, to what extent and how they are cross-regulated remains elusive. Here, we performed orthogonal multi-omics profiling after acute degradation of the largest subunits of Pol I, Pol II, and Pol III, and showed that they mainly affect specific genes. In contrast, the loss of Pol I or Pol II causes few changes for other RNA polymerases and confirms those known. The changes of Pol II transcription after Pol III depletion are the largest among all the cross-regulatory types. Meta-analyses reveal that Pol III depletion increases nucleosome positioning, reduces the FACT complex occupancy, and perturbs Pol II elongation for nearby mRNA genes. Furthermore, the nucleosome positioning changes also underpinning the Pol II effects on Pol III-mediated tRNA transcription. Our results suggest that Pol III works together with Pol II to coordinate their transcription activities by maintaining local chromatin architecture.
2022-11-07 | GSE181696 | GEO
Project description:Genome binding/occupancy profiling by high throughput sequencing ｜ Expression profiling by high throughput sequencing | Other Mammalian nuclei contain Pol I, Pol II, and Pol III. However, to what extent and how they are cross-regulated remains elusive. Here, we performed orthogonal multi-omics profiling after acute degradation of the largest subunits of Pol I, Pol II, and Pol III, and showed that they mainly affect specific genes. In contrast, the loss of Pol I or Pol II causes few changes for other RNA polymerases and confirms those known. The changes of Pol II transcription after Pol III depletion are the largest among all the cross-regulatory types. Meta-analyses reveal that Pol III depletion increases nucleosome positioning, reduces the FACT complex occupancy, and perturbs Pol II elongation for nearby mRNA genes. Furthermore, the nucleosome positioning changes also underpinning the Pol II effects on Pol III-mediated tRNA transcription. Our results suggest that Pol III works together with Pol II to coordinate their transcription activities by maintaining local chromatin architecture.
2022-11-07 | GSE181699 | GEO
Project description:Genome binding/occupancy profiling by high throughput sequencing ｜ Expression profiling by high throughput sequencing | Other Mammalian nuclei contain Pol I, Pol II, and Pol III. However, to what extent and how they are cross-regulated remains elusive. Here, we performed orthogonal multi-omics profiling after acute degradation of the largest subunits of Pol I, Pol II, and Pol III, and showed that they mainly affect specific genes. In contrast, the loss of Pol I or Pol II causes few changes for other RNA polymerases and confirms those known. The changes of Pol II transcription after Pol III depletion are the largest among all the cross-regulatory types. Meta-analyses reveal that Pol III depletion increases nucleosome positioning, reduces the FACT complex occupancy, and perturbs Pol II elongation for nearby mRNA genes. Furthermore, the nucleosome positioning changes also underpinning the Pol II effects on Pol III-mediated tRNA transcription. Our results suggest that Pol III works together with Pol II to coordinate their transcription activities by maintaining local chromatin architecture.
2022-11-07 | GSE181698 | GEO
Project description:Genome binding/occupancy profiling by high throughput sequencing ｜ Expression profiling by high throughput sequencing | Other Mammalian nuclei contain Pol I, Pol II, and Pol III. However, to what extent and how they are cross-regulated remains elusive. Here, we performed orthogonal multi-omics profiling after acute degradation of the largest subunits of Pol I, Pol II, and Pol III, and showed that they mainly affect specific genes. In contrast, the loss of Pol I or Pol II causes few changes for other RNA polymerases and confirms those known. The changes of Pol II transcription after Pol III depletion are the largest among all the cross-regulatory types. Meta-analyses reveal that Pol III depletion increases nucleosome positioning, reduces the FACT complex occupancy, and perturbs Pol II elongation for nearby mRNA genes. Furthermore, the nucleosome positioning changes also underpinning the Pol II effects on Pol III-mediated tRNA transcription. Our results suggest that Pol III works together with Pol II to coordinate their transcription activities by maintaining local chromatin architecture.
2022-11-07 | GSE181697 | GEO
Project description:RSC (Remodels the Structure of Chromatin) is a conserved ATP-dependent chromatin remodeling complex that regulates many biological processes, including transcription by RNA polymerase II (Pol II). We report that not only RSC binds to nucleosomes in coding sequences (CDSs) but also remodels them to promote transcription. RSC MNase ChIP-seq data revealed that RSC-protected fragments were very heterogenous (~80 bp to 180 bp) compared to the sharper profile displayed by the MNase inputs (140 bp to 160 bp), supporting the idea that RSC activity promotes accessibility of nucleosomal DNA. Importantly, RSC binding to +1 nucleosomes and CDSs, but not with -1 nucleosomes, strongly correlated with Pol II occupancies suggesting that the RSC enrichment in CDSs is important for efficient transcription. This is further supported by a similar heterogenous distribution of Pol II-protected fragments. As such, the genes harboring high-levels of RSC in their CDSs were the most strongly affected by ablating RSC function. Altogether, this study provides a mechanism by which RSC-mediated remodeling aids in RNA Pol II traversal though coding sequence nucleosomes in vivo.
2021-04-21 | GSE147065 | GEO
Project description:RSC (remodels the structure of chromatin) is an essential ATP-dependent chromatin remodeling complex in Saccharomyces cerevisiae. The catalytic subunit of RSC, Sth1 uses its ATPase activity to slide or remove nucleosomes. RSC has been shown to regulate the width of the nucleosome-depleted regions (NDRs) by sliding the flanking nucleosomes away from NDRs. As such the nucleosomes encroach NDRs when RSC is depleted and leads to transcription initiation defects. In this study, we examined the effects of the catalytic-dead Sth1 on transcription and compared them to the effects observed during acute and rapid Sth1 depletion by auxin-induced degron strategy. We found that rapid depletion of Sth1 reduces recruitment of TBP and Pol II in highly transcribed genes, as would be expected considering its role in regulating chromatin structure at promoters. In contrast, cells harboring the catalytic-dead Sth1 exhibited a severe reduction in TBP binding, but surprisingly, also displayed a substantial accumulation in Pol II occupancies within coding regions. After depleting endogenous Sth1 in the catalytic dead mutant, we observed a further increase in Pol II occupancies, suggesting that the inactive Sth1 contributed to the observed accumulation of Pol II in coding regions. Notwithstanding the Pol II increase, the ORF occupancies of histone chaperones FACT and Spt6 were significantly reduced in the mutant. These results suggest a potential role for RSC in recruiting/retaining these chaperones in coding regions. Pol II accumulation despite substantial reductions in TBP, FACT, and Spt6 occupancies in the catalytic-dead mutant could be indicative of severe transcription elongation and termination defects. Such defects would be consistent with studies showing that RSC is recruited to coding regions in a transcription-dependent manner. Thus, these findings imply a role for RSC in transcription elongation and termination processes, in addition to its established role in transcription initiation.
2023-11-07 | GSE245521 | GEO
Project description:Most yeast genes have a nucleosome-depleted region (NDR) at the promoter and an array of regularly spaced nucleosomes phased relative to the transcription start site. We have examined the interplay between RSC (a conserved essential SWI/SNF-type complex that determines NDR size) and the ISW1, CHD1 and ISW2 nucleosome spacing enzymes in chromatin organization and transcription, using isogenic strains lacking all combinations of these enzymes. The contributions of these remodelers to chromatin organization are largely combinatorial, distinct and non-redundant, supporting a model in which the +1 nucleosome is positioned by RSC and then used as a reference nucleosome by the spacing enzymes. Defective chromatin organization correlates with altered RNA polymerase II (Pol II) distribution. RSC-depleted cells exhibit low levels of elongating Pol II and high levels of terminating Pol II, consistent with defects in both termination and initiation, suggesting that RSC facilitates both. Cells lacking both ISW1 and CHD1 show the opposite Pol II distribution, suggesting elongation and termination defects. These cells have extremely disrupted chromatin, with high levels of close-packed di-nucleosomes near the 5’-ends of genes. We propose that ISW1 and CHD1 facilitate Pol II elongation by separating close-packed nucleosomes and by eliminating long linkers to prevent cryptic initiation.
2019-01-16 | GSE117514 | GEO