Nucleosome Cores and Histone H1 in the Binding of GAL4 Derivatives and the Reactivation of Transcription from Nucleosome Templates In Vitro

Juan, Li‐Jung; Walter, Phillip; Taylor, Ian; Kingston, Robert E.; Workman, Jerry L.

doi:10.1101/sqb.1993.058.01.026

Cited by 13 publications

(6 citation statements)

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“…It has been known for many years that the binding of multiple transcription factors to nucleosomes occurs in a "cooperative" manner and results in destabilization of the underlying nucleosome (Taylor et al 1991;Workman and Kingston 1992;Juan et al 1993;Morse 1993;Owen-Hughes and Workman 1996;Avolio-Hunter et al 2001). In addition, nucleosome remodeling complexes of the SWI/SNF family (e.g., SWI/ SNF and RSC) have been shown to function in displacing histone octamers from one piece of DNA onto another (Lorch et al 1999), through a mechanism that appears to involve forcing DNA bulges into the nucleosome (for review, see Flaus and Owen-Hughes 2004;Cairns 2005).…”

Section: How Are Nucleosome-free Regions Generated?mentioning

confidence: 99%

Nucleosome displacement in transcription: Figure 1.

Workman¹

2006

Genes Dev.

277

221

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Recent reports reinforce the notion that nucleosomes are highly dynamic in response to the process of transcription. Nucleosomes are displaced at promoters during gene activation in a process that involves histone modification, ATP-dependent nucleosome remodeling complexes, histone chaperones and perhaps histone variants. During transcription elongation nucleosomes are acetylated and transferred behind RNA polymerase II where they are required to suppress spurious transcription initiation within the body of the gene. It is becoming increasingly clear that the eukaryotic transcriptional machinery is adapted to exploit the presence of nucleosomes in very sophisticated ways. Nucleosome-free regions at gene promotersRemoval of nucleosomes has been a long-standing hypothesis for how genes might become activated, but only recently have experiments begun to rigorously address this topic. For some time after the discovery of DNasehypersensitive sites (DHSs) in chromatin (for review, see Elgin 1981), it was anticipated that these nuclease sensitive regions would correspond to segments along the chromosome that are free of nucleosomes. With the common occurrence of DHSs at known transcriptional regulatory regions such as enhancers and promoters, mapping these exposed sites in genomic DNA became a powerful tool for identifying novel regulatory sites such as locus control regions (LCRs) and other functional genomic sequences (for review see, Gross and Garrard 1988). However, the question of whether these sites were actually histone free or simply did not look like nucleosomes to nucleases remained unresolved. The initial idea that DHSs must be nucleosome-free was attractive since the structure and stability of nucleosomes did not seem likely to accommodate the cobinding of transcription factors (Brown 1984;Kornberg and Lorch 1991). Early support for the notion that at least some of these regions are free of histones came from McGhee and Felsenfeld (McGhee et al. 1981), who examined the chicken adult ␤-globin DHS by restriction endonuclease digestion. They showed the release of a 115-base-pair (bp) fragment from the DHS, of which one-third migrated on gels like naked DNA. In contrast, studies of an inducible DHS at the MMTV promoter suggested that it was still occupied by core histones following induction (Bresnick et al. 1992;Truss et al. 1995), thereby demonstrating the co-occupancy of histones and transcription factors. Moreover, a DHS could be reconstituted by the binding of transcription factors to the HIV-1 enhancer within a nucleosome array without the loss of histones (Steger and Workman 1997;Angelov et al. 2000). Thus, while DHSs do not appear to contain canonical nucleosomes as defined by nuclease digestion, an altered nucleosome or alternative histone DNA complex may still exist at these sites in some instances. Nevertheless, remembering the caveat that DHSs might still be bound by histones, we will refer to these sites as nucleosome-free for the purposes of this review. Nucleosome distribution in Saccharomyces ce...

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Section: How Are Nucleosome-free Regions Generated?mentioning

confidence: 99%

Nucleosome displacement in transcription: Figure 1.

Workman¹

2006

Genes Dev.

277

221

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“…DNA beyond the 146 bp contained in the nucleosome core; Ref. 31) indicates that correct binding of the central globular domain is crucial to mediating the repressive actions of H1.…”

Section: Discussionmentioning

confidence: 99%

H1-mediated Repression of Transcription Factor Binding to a Stably Positioned Nucleosome

Juan

Utley

Vignali

et al. 1997

Journal of Biological Chemistry

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Biochemical studies have implicated both nucleosome core assembly and/or the subsequent binding of the linker histone H1 in transcriptional repression (4 -9). Because the affinities of sequence-specific DNA-binding proteins for nucleosomal DNA are often dramatically reduced compared with free DNA (reviewed in Ref. 10), nucleosomes repress the transcriptional process, at least in part, by inhibiting access of activator proteins to their cognate binding sites in chromatin. Factor occupancy of binding sites in nucleosomal arrays is most likely achieved through multiple mechanisms involving nucleosome disruption, nucleosome displacement in trans, or histone octamer sliding in cis (reviewed in Ref. 11). The idea of mobile nucleosomes (i.e. nucleosome sliding) is attractive in that it has the potential to create transient accessibility of factors to their binding sites. Its potential importance is further implicated in studies that illustrate the differential affinity of factors for sites at different translational and rotational positions within nucleosomes (12-15). Using a model system consisting of chromatin assembled on tandemly repeated sea urchin 5 S rRNA nucleosome positioning sequences (16), Bradbury and colleagues (17, 18) have previously reported that nucleosomes adopt a dominant position surrounded by minor positions 10 base pairs apart (i.e. in the same rotational frame). These data indicate that the cluster of octamer positions is in dynamic equilibrium in low ionic strength conditions. In the presence of the linker histone H1, this mobility is inhibited (19). The same group found that this short range sliding behavior also applies to bulk mononucleosomes and nucleosomes reconstituted onto sequences of the Alu family of ubiquitous repeats. Thus, they proposed that nucleosome mobility is a general behavior (20). Moreover, H1-mediated reduction in nucleosome mobility has been implicated in repression of transcription of a dinucleosome reconstituted onto a dimerized Xenopus somatic 5 S rRNA gene (2).In our previous studies, we reported for the first time direct inhibition of factor binding by the association of H1 with nucleosome cores. The binding of H1 to form a chromatosome significantly repressed the subsequent binding of USF 1 but only slightly inhibited GAL4-AH binding (1). In this report, we extend these studies to explore the underlying mechanisms by which H1 repressed USF binding. The results illustrate H1-mediated repression of USF binding to a stably positioned nucleosome. Thus, H1 repression in this instance occurred in the absence of nucleosome mobility. In addition, H1 repressed USF binding to a site on the opposite side of the histone octamer from the entry and exit points of the linker DNA. These data are consistent with a mechanism by which H1 stabilizes histone octamer-DNA interactions, thus reducing transient exposure of factor binding sites. MATERIALS AND METHODSPreparation of DNA Probes-The 183-bp probe DNAs, referred to as GU or UG probes, were either directly generated by BamHI digesti...

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“…UASs and their associated TFs are probably required for expression of all protein-coding genes transcribed by Pol II, which contain one or more UASs. Although there is a low level of nonactivator-dependent "basal" transcription in vitro, basal transcription is repressed when a chromatin template, rather than free DNA, is used, suggesting that nucleosomes repress non-TF-dependent transcription initiation in vivo (Juan et al 1993). Thus, the "ground-state" of a yeast promoter is inactive and transcription must be promoted by one or more TFs (Struhl 1999).…”

Section: Upstream Activation Sequence Elementsmentioning

confidence: 99%

Transcriptional Regulation inSaccharomyces cerevisiae: Transcription Factor Regulation and Function, Mechanisms of Initiation, and Roles of Activators and Coactivators

2011

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Here we review recent advances in understanding the regulation of mRNA synthesis in Saccharomyces cerevisiae. Many fundamental gene regulatory mechanisms have been conserved in all eukaryotes, and budding yeast has been at the forefront in the discovery and dissection of these conserved mechanisms. Topics covered include upstream activation sequence and promoter structure, transcription factor classification, and examples of regulated transcription factor activity. We also examine advances in understanding the RNA polymerase II transcription machinery, conserved coactivator complexes, transcription activation domains, and the cooperation of these factors in gene regulatory mechanisms. TABLE OF CONTENTS Abstract 705Introduction 706

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Nucleosome Cores and Histone H1 in the Binding of GAL4 Derivatives and the Reactivation of Transcription from Nucleosome Templates In Vitro

Cited by 13 publications

References 0 publications

Nucleosome displacement in transcription: Figure 1.

Nucleosome displacement in transcription: Figure 1.

H1-mediated Repression of Transcription Factor Binding to a Stably Positioned Nucleosome

Transcriptional Regulation inSaccharomyces cerevisiae: Transcription Factor Regulation and Function, Mechanisms of Initiation, and Roles of Activators and Coactivators

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