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Steven Henikoff - One of the best experts on this subject based on the ideXlab platform.
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Nucleosomes remember where they were
Proceedings of the National Academy of Sciences of the United States of America, 2019Co-Authors: Steven Henikoff, Kami AhmadAbstract:A central postulate in chromatin biology is that Nucleosomes are inherited through replication, and evidence for the recycling of Nucleosomes from ahead of the replication fork to behind goes back more than 40 y (1, 2). Early electron microscopic observations of chromatin fibers revealed that Nucleosomes form directly behind the replication fork (3), confirmed by later kinetic studies (4). However, it has remained uncertain as to whether histones from a Nucleosome ahead of the fork return to the same position on a daughter strand after the fork has passed through. This is a critical question to resolve, because any dispersion of histones behind the fork disperses histone features such as posttranslational modifications that have been causally implicated in the propagation of gene expression states (5). The restoration of Nucleosome positions may also be important for transcriptional regulation, given that Nucleosomes act as barriers to transcriptional elongation but are disrupted when RNA polymerase passes through (6). Thus both replication and transcription can potentially disperse Nucleosomes. To address this uncertainty, Schlissel and Rine (7) devise an elegant strategy to permanently mark histones within a 4-Nucleosome region of the budding yeast genome, which allows them to precisely determine whether or not those Nucleosomes shift positions after replication fork passage. By engineering the marked region within the repressible and inducible GAL10 gene, this system also allows them to separate the effects of replication fork passage and transcription on Nucleosome positioning. Biochemical studies have examined the process of Nucleosome redeposition postreplication, but the question of positional memory has not been resolved. Unwinding of a Nucleosome in vitro by the action of a helicase and a DNA polymerase resulted in transfer of the histone core to the leading-strand DNA duplex (8). As the leading strand is replicated before the lagging strand in vivo, a similar … [↵][1]1To whom correspondence may be addressed. Email: steveh{at}fhcrc.org. [1]: #xref-corresp-1-1
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Nucleosomes remember where they were
Proceedings of the National Academy of Sciences of the United States of America, 2019Co-Authors: Steven Henikoff, Kami AhmadAbstract:A central postulate in chromatin biology is that Nucleosomes are inherited through replication, and evidence for the recycling of Nucleosomes from ahead of the replication fork to behind goes back more than 40 y (1, 2). Early electron microscopic observations of chromatin fibers revealed that Nucleosomes form directly behind the replication fork (3), confirmed by later kinetic studies (4). However, it has remained uncertain as to whether histones from a Nucleosome ahead of the fork return to the same position on a daughter strand after the fork has passed through. This is a critical question to resolve, because any dispersion of histones behind the fork disperses histone features such as posttranslational modifications that have been causally implicated in the propagation of gene expression states (5). The restoration of Nucleosome positions may also be important for transcriptional regulation, given that Nucleosomes act as barriers to transcriptional elongation but are disrupted when RNA polymerase passes through (6). Thus both replication and transcription can potentially disperse Nucleosomes. To address this uncertainty, Schlissel and Rine (7) devise an elegant strategy to permanently mark histones within a 4-Nucleosome region of the budding yeast genome, which allows them to precisely determine whether or not those Nucleosomes shift positions after replication fork passage. By engineering the marked region within the repressible and inducible GAL10 gene, this system also allows them to separate the effects of replication fork passage and transcription on Nucleosome positioning. Biochemical studies have examined the process of Nucleosome redeposition postreplication, but the question of positional memory has not been resolved. Unwinding of a Nucleosome in vitro by the action of a helicase and a DNA polymerase resulted in transfer of the histone core to the leading-strand DNA duplex (8). As the leading strand is replicated before the lagging strand in vivo, a similar … [↵][1]1To whom correspondence may be addressed. Email: steveh{at}fhcrc.org. [1]: #xref-corresp-1-1
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precise genome wide mapping of single Nucleosomes and linkers in vivo
Genome Biology, 2018Co-Authors: Răzvan V Chereji, Srinivas Ramachandran, Terri D Bryson, Steven HenikoffAbstract:We developed a chemical cleavage method that releases single Nucleosome dyad-containing fragments, allowing us to precisely map both single Nucleosomes and linkers with high accuracy genome-wide in yeast. Our single Nucleosome positioning data reveal that Nucleosomes occupy preferred positions that differ by integral multiples of the DNA helical repeat. By comparing Nucleosome dyad positioning maps to existing genomic and transcriptomic data, we evaluated the contributions of sequence, transcription, and histones H1 and H2A.Z in defining the chromatin landscape. We present a biophysical model that neglects DNA sequence and shows that steric occlusion suffices to explain the salient features of Nucleosome positioning.
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Replicating Nucleosomes.
Science advances, 2015Co-Authors: Srinivas Ramachandran, Steven HenikoffAbstract:Eukaryotic replication disrupts each Nucleosome as the fork passes, followed by re-assembly of disrupted Nucleosomes and incorporation of newly synthesized histones into Nucleosomes in the daughter genomes. In this review, we examine this process of replication-coupled Nucleosome assembly to understand how characteristic steady state Nucleosome landscapes are attained. Recent studies have begun to elucidate mechanisms involved in histone transfer during replication and maturation of the Nucleosome landscape after disruption by replication. A fuller understanding of replication-coupled Nucleosome assembly will be needed to explain how epigenetic information is replicated at every cell division.
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asymmetric Nucleosomes flank promoters in the budding yeast genome
Genome Research, 2015Co-Authors: Srinivas Ramachandran, Gabriel E Zentner, Steven HenikoffAbstract:Nucleosomes in active chromatin are dynamic, but whether they have distinct structural conformations is unknown. To identify Nucleosomes with alternative structures genome-wide, we used H4S47C-anchored cleavage mapping, which revealed that 5% of budding yeast (Saccharomyces cerevisiae) Nucleosome positions have asymmetric histone-DNA interactions. These asymmetric interactions are enriched at Nucleosome positions that flank promoters. Micrococcal nuclease (MNase) sequence-based profiles of asymmetric Nucleosome positions revealed a corresponding asymmetry in MNase protection near the dyad axis, suggesting that the loss of DNA contacts around H4S47 is accompanied by protection of the DNA from MNase. Chromatin immunoprecipitation mapping of selected Nucleosome remodelers indicated that asymmetric Nucleosomes are bound by the RSC chromatin remodeling complex, which is required for maintaining Nucleosomes at asymmetric positions. These results imply that the asymmetric Nucleosome-RSC complex is a metastable intermediate representing partial unwrapping and protection of nucleosomal DNA on one side of the dyad axis during chromatin remodeling.
Franklin B Pugh - One of the best experts on this subject based on the ideXlab platform.
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genome wide Nucleosome specificity and directionality of chromatin remodelers
Cell, 2012Co-Authors: Kuangyu Yen, Vinesh Vinayachandran, Thomas R Koerber, Kiran Batta, Franklin B PughAbstract:Summary How chromatin remodelers cooperate to organize Nucleosomes around the start and end of genes is not known. We determined the genome-wide binding of remodeler complexes SWI/SNF, RSC, ISW1a, ISW1b, ISW2, and INO80 to individual Nucleosomes in Saccharomyces , and determined their functional contributions to Nucleosome positioning through deletion analysis. We applied ultra-high-resolution ChIP-exo mapping to Isw2 to determine its subnucleosomal orientation and organization on a genomic scale. Remodelers interacted with selected Nucleosome positions relative to the start and end of genes and produced net directionality in moving Nucleosomes either away or toward Nucleosome-free regions at the 5′ and 3′ ends of genes. Isw2 possessed a subnucleosomal organization in accord with biochemical and crystallographic-based models that place its linker binding region within promoters and abutted against Reb1-bound locations. Together, these findings reveal a coordinated position-specific approach taken by remodelers to organize genic Nucleosomes into arrays.
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interaction of transcriptional regulators with specific Nucleosomes across the saccharomyces genome
Molecular Cell, 2009Co-Authors: Thomas R Koerber, Cizhong Jiang, Ho Sung Rhee, Franklin B PughAbstract:A canonical Nucleosome architecture around promoters establishes the context in which proteins regulate gene expression. Whether gene regulatory proteins that interact with Nucleosomes are selective for individual Nucleosome positions across the genome is not known. Here, we examine on a genomic scale several protein-Nucleosome interactions, including those that (1) bind histones (Bdf1/SWR1 and Srm1), (2) bind specific DNA sequences (Rap1 and Reb1), and (3) potentially collide with Nucleosomes during transcription (RNA polymerase II). We find that the Bdf1/SWR1 complex forms a diNucleosome complex that is selective for the +1 and +2 Nucleosomes of active genes. Rap1 selectively binds to its cognate site on the rotationally exposed first and second helical turn of nucleosomal DNA. We find that a transcribing RNA polymerase creates a delocalized state of resident Nucleosomes. These findings suggest that Nucleosomes around promoter regions have position-specific functions and that some gene regulators have position-specific nucleosomal interactions.
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Nucleosome positioning and gene regulation advances through genomics
Nature Reviews Genetics, 2009Co-Authors: Cizhong Jiang, Franklin B PughAbstract:Knowing the precise locations of Nucleosomes in a genome is key to understanding how genes are regulated. Recent 'next generation' ChIP-chip and ChIP-Seq technologies have accelerated our understanding of the basic principles of chromatin organization. Here we discuss what high-resolution genome-wide maps of Nucleosome positions have taught us about how Nucleosome positioning demarcates promoter regions and transcriptional start sites, and how the composition and structure of promoter Nucleosomes facilitate or inhibit transcription. A detailed picture is starting to emerge of how diverse factors, including underlying DNA sequences and chromatin remodelling complexes, influence Nucleosome positioning.
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a barrier Nucleosome model for statistical positioning of Nucleosomes throughout the yeast genome
Genome Research, 2008Co-Authors: Travis N Mavrich, Ilya Ioshikhes, Bryan J Venters, Cizhong Jiang, Lynn P Tomsho, Stephan C Schuster, Istvan Albert, Ji Qi, Franklin B PughAbstract:Most Nucleosomes are well-organized at the 5′ ends of S. cerevisiae genes where “−1” and “+1” Nucleosomes bracket a Nucleosome-free promoter region (NFR). How nucleosomal organization is specified by the genome is less clear. Here we establish and inter-relate rules governing genomic Nucleosome organization by sequencing DNA from more than one million immunopurified S. cerevisiae Nucleosomes (displayed at http://atlas.bx.psu.edu/). Evidence is presented that the organization of Nucleosomes throughout genes is largely a consequence of statistical packing principles. The genomic sequence specifies the location of the −1 and +1 Nucleosomes. The +1 Nucleosome forms a barrier against which Nucleosomes are packed, resulting in uniform positioning, which decays at farther distances from the barrier. We present evidence for a novel 3′ NFR that is present at >95% of all genes. 3′ NFRs may be important for transcription termination and anti-sense initiation. We present a high-resolution genome-wide map of TFIIB locations that implicates 3′ NFRs in gene looping.
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translational and rotational settings of h2a z Nucleosomes across the saccharomyces cerevisiae genome
Nature, 2007Co-Authors: Istvan Albert, Travis N Mavrich, Lynn P Tomsho, Stephan C Schuster, Sara J Zanton, Ji Qi, Franklin B PughAbstract:The Nucleosome is the fundamental building block of eukaryotic chromosomes. Access to genetic information encoded in chromosomes is dependent on the position of Nucleosomes along the DNA. Alternative locations just a few nucleotides apart can have profound effects on gene expression1. Yet the nucleosomal context in which chromosomal and gene regulatory elements reside remains ill-defined on a genomic scale. Here we sequence the DNA of 322,000 individual Saccharomyces cerevisiae Nucleosomes, containing the histone variant H2A.Z, to provide a comprehensive map of H2A.Z Nucleosomes in functionally important regions. With a median 4-base-pair resolution, we identify new and established signatures of Nucleosome positioning. A single predominant rotational setting and multiple translational settings are evident. Chromosomal elements, ranging from telomeres to centromeres and transcriptional units, are found to possess characteristic nucleosomal architecture that may be important for their function. Promoter regulatory elements, including transcription factor binding sites and transcriptional start sites, show topological relationships with Nucleosomes, such that transcription factor binding sites tend to be rotationally exposed on the Nucleosome surface near its border. Transcriptional start sites tended to reside about one helical turn inside the Nucleosome border. These findings reveal an intimate relationship between chromatin architecture and the underlying DNA sequence it regulates.
Alan G Hinnebusch - One of the best experts on this subject based on the ideXlab platform.
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chromatin remodeler ino80c acts independently of h2a z to evict promoter Nucleosomes and stimulate transcription of highly expressed genes in yeast
Nucleic Acids Research, 2020Co-Authors: Emily Biernat, Răzvan V Chereji, Yashpal Rawal, David J Clark, Chhabi K Govind, Alan G HinnebuschAbstract:The chromatin remodelers SWI/SNF and RSC function in evicting promoter Nucleosomes at highly expressed yeast genes, particularly those activated by transcription factor Gcn4. Ino80 remodeling complex (Ino80C) can establish Nucleosome-depleted regions (NDRs) in reconstituted chromatin, and was implicated in removing histone variant H2A.Z from the -1 and +1 Nucleosomes flanking NDRs; however, Ino80C's function in transcriptional activation in vivo is not well understood. Analyzing the cohort of Gcn4-induced genes in ino80Δ mutants has uncovered a role for Ino80C on par with SWI/SNF in evicting promoter Nucleosomes and transcriptional activation. Compared to SWI/SNF, Ino80C generally functions over a wider region, spanning the -1 and +1 Nucleosomes, NDR and proximal genic Nucleosomes, at genes highly dependent on its function. Defects in Nucleosome eviction in ino80Δ cells are frequently accompanied by reduced promoter occupancies of TBP, and diminished transcription; and Ino80 is enriched at genes requiring its remodeler activity. Importantly, nuclear depletion of Ino80 impairs promoter Nucleosome eviction even in a mutant lacking H2A.Z. Thus, Ino80C acts widely in the yeast genome together with RSC and SWI/SNF in evicting promoter Nucleosomes and enhancing transcription, all in a manner at least partly independent of H2A.Z editing.
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swi snf and rsc cooperate to reposition and evict promoter Nucleosomes at highly expressed genes in yeast
Genes & Development, 2018Co-Authors: Yashpal Rawal, Răzvan V Chereji, Sudha Ananthakrishnan, David J Clark, Chhabi K Govind, Alan G HinnebuschAbstract:: The Nucleosome remodeling complex RSC functions throughout the yeast genome to set the positions of -1 and +1 Nucleosomes and thereby determines the widths of Nucleosome-depleted regions (NDRs). The related complex SWI/SNF participates in Nucleosome remodeling/eviction and promoter activation at certain yeast genes, including those activated by transcription factor Gcn4, but did not appear to function broadly in establishing NDRs. By analyzing the large cohort of Gcn4-induced genes in mutants lacking the catalytic subunits of SWI/SNF or RSC, we uncovered cooperation between these remodelers in evicting Nucleosomes from different locations in the promoter and repositioning the +1 Nucleosome downstream to produce wider NDRs-highly depleted of Nucleosomes-during transcriptional activation. SWI/SNF also functions on a par with RSC at the most highly transcribed constitutively expressed genes, suggesting general cooperation by these remodelers for maximal transcription. SWI/SNF and RSC occupancies are greatest at the most highly expressed genes, consistent with their cooperative functions in Nucleosome remodeling and transcriptional activation. Thus, SWI/SNF acts comparably with RSC in forming wide Nucleosome-free NDRs to achieve high-level transcription but only at the most highly expressed genes exhibiting the greatest SWI/SNF occupancies.
Philipp Korber - One of the best experts on this subject based on the ideXlab platform.
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Nucleosome positioning in yeasts: methods, maps, and mechanisms
Chromosoma, 2015Co-Authors: Corinna Lieleg, Nils Krietenstein, Maria Walker, Philipp KorberAbstract:Eukaryotic nuclear DNA is packaged into Nucleosomes. During the past decade, genome-wide Nucleosome mapping across species revealed the high degree of order in Nucleosome positioning. There is a conserved stereotypical Nucleosome organization around transcription start sites (TSSs) with a Nucleosome-depleted region (NDR) upstream of the TSS and a TSS-aligned regular array of evenly spaced Nucleosomes downstream over the gene body. As Nucleosomes largely impede access to DNA and thereby provide an important level of genome regulation, it is of general interest to understand the mechanisms generating Nucleosome positioning and especially the stereotypical NDR-array pattern. We focus here on the most advanced models, unicellular yeasts, and review the progress in mapping Nucleosomes and which Nucleosome positioning mechanisms are discussed. There are four mechanistic aspects: How are NDRs generated? How are individual Nucleosomes positioned, especially those flanking the NDRs? How are Nucleosomes evenly spaced leading to regular arrays? How are regular arrays aligned at TSSs? The main candidates for Nucleosome positioning determinants are intrinsic DNA binding preferences of the histone octamer, specific DNA binding factors, Nucleosome remodeling enzymes, transcription, and statistical positioning. We summarize the state of the art in an integrative model where Nucleosomes are positioned by a combination of all these candidate determinants. We highlight the predominance of active mechanisms involving Nucleosome remodeling enzymes which may be recruited by DNA binding factors and the transcription machinery. While this mechanistic framework emerged clearly during recent years, the involved factors and their mechanisms are still poorly understood and require future efforts combining in vivo and in vitro approaches.
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Nucleosome spacing generated by ISWI and CHD1 remodelers is constant regardless of Nucleosome density.
Molecular and Cellular Biology, 2015Co-Authors: Corinna Lieleg, Philip Ketterer, Johanna Ludwigsen, Hendrik Dietz, Felix Mueller-planitz, Johannes Nuebler, Ulrich Gerland, Philipp KorberAbstract:Arrays of regularly spaced Nucleosomes are a hallmark of chromatin, but it remains unclear how they are generated. Recent genome-wide studies, in vitro and in vivo, showed constant Nucleosome spacing even if the histone concentration was experimentally reduced. This counters the long-held assumption that Nucleosome density determines spacing and calls for factors keeping spacing constant regardless of Nucleosome density. We call this a clamping activity. Here, we show in a purified system that ISWI- and CHD1-type Nucleosome remodelers have a clamping activity such that they not only generate regularly spaced Nucleosome arrays but also generate constant spacing regardless of Nucleosome density. This points to a functionally attractive Nucleosome interaction that could be mediated either directly by Nucleosome-Nucleosome contacts or indirectly through the remodelers. Mutant Drosophila melanogaster ISWI without the HAND-SANT-SLIDE (HSS) domain had no detectable spacing activity even though it is known to remodel and slide Nucleosomes. This suggests that the role of ISWI remodelers in generating constant spacing is not just to mediate Nucleosome sliding; they actively contribute to the attractive interaction. Additional factors are necessary to set physiological spacing in absolute terms.
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Replication-guided Nucleosome packing and Nucleosome breathing expedite the formation of dense arrays
Nucleic Acids Research, 2014Co-Authors: Brendan Osberg, Philipp Korber, Johannes Nuebler, Ulrich GerlandAbstract:The first level of genome packaging in eukaryotic cells involves the formation of dense Nucleosome arrays, with DNA coverage near 90% in yeasts. How cells achieve such high coverage within a short time, e.g. after DNA replication, remains poorly understood. It is known that random sequential adsorption of impenetrable particles on a line reaches high densityextremelyslowly,duetoajammingphenomenon. The Nucleosome-shifting action of remodeling enzymes has been proposed as a mechanism to resolve such jams. Here, we suggest two biophysical mechanisms which assist rapid filling of DNA with Nucleosomes, and we quantitatively characterize these mechanisms within mathematical models. First, we show that the ‘softness’ of Nucleosomes, due to Nucleosome breathing and stepwise Nucleosome assembly, significantly alters the filling behavior, speeding up the process relative to ‘hard’ particles with fixed, mutually exclusive DNA footprints. Second, we explore model scenarios in which the progression of the replication fork could eliminate Nucleosome jamming, either by rapid filling in its wake or via memory of the parental Nucleosome positions. Taken together, our results suggest that biophysical effects promote rapid Nucleosome filling, making the reassembly of densely packed Nucleosomes after DNA replication a simpler task for cells than was previously thought.
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schizosaccharomyces pombe genome wide Nucleosome mapping reveals positioning mechanisms distinct from those of saccharomyces cerevisiae
Nature Structural & Molecular Biology, 2010Co-Authors: Alexandra Lantermann, Guocheng Yuan, Tobias Straub, Annelie Stralfors, Karl Ekwall, Philipp KorberAbstract:Nucleosome occupancy can affect the accessibility of DNA to other factors. A genome-wide map of Nucleosomes in Schizosaccharomyces pombe is now presented. Comparisons to published Saccharomyces cerevisiae maps reveal species-specific differences arguing for evolutionary plasticity of Nucleosome positioning mechanisms. Positioned Nucleosomes limit the access of proteins to DNA and implement regulatory features encoded in eukaryotic genomes. Here we have generated the first genome-wide Nucleosome positioning map for Schizosaccharomyces pombe and annotated transcription start and termination sites genome wide. Using this resource, we found surprising differences from the previously published Nucleosome organization of the distantly related yeast Saccharomyces cerevisiae. DNA sequence guides Nucleosome positioning differently: for example, poly(dA-dT) elements are not enriched in S. pombe Nucleosome-depleted regions. Regular nucleosomal arrays emanate more asymmetrically—mainly codirectionally with transcription—from promoter Nucleosome-depleted regions, but promoters harboring the histone variant H2A.Z also show regular arrays upstream of these regions. Regular Nucleosome phasing in S. pombe has a very short repeat length of 154 base pairs and requires a remodeler, Mit1, that is conserved in humans but is not found in S. cerevisiae. Nucleosome positioning mechanisms are evidently not universal but evolutionarily plastic.
Răzvan V Chereji - One of the best experts on this subject based on the ideXlab platform.
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chromatin remodeler ino80c acts independently of h2a z to evict promoter Nucleosomes and stimulate transcription of highly expressed genes in yeast
Nucleic Acids Research, 2020Co-Authors: Emily Biernat, Răzvan V Chereji, Yashpal Rawal, David J Clark, Chhabi K Govind, Alan G HinnebuschAbstract:The chromatin remodelers SWI/SNF and RSC function in evicting promoter Nucleosomes at highly expressed yeast genes, particularly those activated by transcription factor Gcn4. Ino80 remodeling complex (Ino80C) can establish Nucleosome-depleted regions (NDRs) in reconstituted chromatin, and was implicated in removing histone variant H2A.Z from the -1 and +1 Nucleosomes flanking NDRs; however, Ino80C's function in transcriptional activation in vivo is not well understood. Analyzing the cohort of Gcn4-induced genes in ino80Δ mutants has uncovered a role for Ino80C on par with SWI/SNF in evicting promoter Nucleosomes and transcriptional activation. Compared to SWI/SNF, Ino80C generally functions over a wider region, spanning the -1 and +1 Nucleosomes, NDR and proximal genic Nucleosomes, at genes highly dependent on its function. Defects in Nucleosome eviction in ino80Δ cells are frequently accompanied by reduced promoter occupancies of TBP, and diminished transcription; and Ino80 is enriched at genes requiring its remodeler activity. Importantly, nuclear depletion of Ino80 impairs promoter Nucleosome eviction even in a mutant lacking H2A.Z. Thus, Ino80C acts widely in the yeast genome together with RSC and SWI/SNF in evicting promoter Nucleosomes and enhancing transcription, all in a manner at least partly independent of H2A.Z editing.
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swi snf and rsc cooperate to reposition and evict promoter Nucleosomes at highly expressed genes in yeast
Genes & Development, 2018Co-Authors: Yashpal Rawal, Răzvan V Chereji, Sudha Ananthakrishnan, David J Clark, Chhabi K Govind, Alan G HinnebuschAbstract:: The Nucleosome remodeling complex RSC functions throughout the yeast genome to set the positions of -1 and +1 Nucleosomes and thereby determines the widths of Nucleosome-depleted regions (NDRs). The related complex SWI/SNF participates in Nucleosome remodeling/eviction and promoter activation at certain yeast genes, including those activated by transcription factor Gcn4, but did not appear to function broadly in establishing NDRs. By analyzing the large cohort of Gcn4-induced genes in mutants lacking the catalytic subunits of SWI/SNF or RSC, we uncovered cooperation between these remodelers in evicting Nucleosomes from different locations in the promoter and repositioning the +1 Nucleosome downstream to produce wider NDRs-highly depleted of Nucleosomes-during transcriptional activation. SWI/SNF also functions on a par with RSC at the most highly transcribed constitutively expressed genes, suggesting general cooperation by these remodelers for maximal transcription. SWI/SNF and RSC occupancies are greatest at the most highly expressed genes, consistent with their cooperative functions in Nucleosome remodeling and transcriptional activation. Thus, SWI/SNF acts comparably with RSC in forming wide Nucleosome-free NDRs to achieve high-level transcription but only at the most highly expressed genes exhibiting the greatest SWI/SNF occupancies.
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precise genome wide mapping of single Nucleosomes and linkers in vivo
Genome Biology, 2018Co-Authors: Răzvan V Chereji, Srinivas Ramachandran, Terri D Bryson, Steven HenikoffAbstract:We developed a chemical cleavage method that releases single Nucleosome dyad-containing fragments, allowing us to precisely map both single Nucleosomes and linkers with high accuracy genome-wide in yeast. Our single Nucleosome positioning data reveal that Nucleosomes occupy preferred positions that differ by integral multiples of the DNA helical repeat. By comparing Nucleosome dyad positioning maps to existing genomic and transcriptomic data, we evaluated the contributions of sequence, transcription, and histones H1 and H2A.Z in defining the chromatin landscape. We present a biophysical model that neglects DNA sequence and shows that steric occlusion suffices to explain the salient features of Nucleosome positioning.
