Specific regulation of Xenopus chromosomal 5S rRNA gene transcription in vivo by histone H1.

Bouvet, Philippe; Dimitrov, Stéfan; Wolffe, Alan P.

doi:10.1101/gad.8.10.1147

Cited by 233 publications

(170 citation statements)

References 91 publications

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“…Preferential binding of histone H1 has been described for the AT-rich DNA sequences of the SAR (17) as well as the AT-rich flanking sequences of the oocyte-type 5S RNA gene of Xenopus laevis (39), leading to the specific repression of the Xenopus oocyte 5S rRNA gene (6,16). In order to determine if histone H1 could also preferentially bind to the AT-rich DNA sequence present on the upstream region of the IFN-␤ promoter, we carried out a series of photofootprinting analyses of the muIFN-␤ promoter in the presence and absence of histone H1.…”

Section: High-affinity Binding Of the Hmgi Protein To The Upstream Atmentioning

confidence: 99%

Specific Binding of High-Mobility-Group I (HMGI) Protein and Histone H1 to the Upstream AT-Rich Region of the Murine Beta Interferon Promoter: HMGI Protein Acts as a Potential Antirepressor of the Promoter

Bonnefoy

Bandu

Doly

1999

Molecular and Cellular Biology

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The high-mobility-group I (HMGI) protein is a nonhistone component of active chromatin. In this work, we demonstrate that HMGI protein specifically binds to the AT-rich region of the murine beta interferon (IFN-␤) promoter localized upstream of the murine virus-responsive element (VRE). Contrary to what has been described for the human promoter, HMGI protein did not specifically bind to the VRE of the murine IFN-␤ promoter. Stably transfected promoters carrying mutations on this HMGI binding site displayed delayed virusinduced kinetics of transcription. When integrated into chromatin, the mutated promoter remained repressed and never reached normal transcriptional activity. Such a phenomenon was not observed with transiently transfected promoters upon which chromatin was only partially reconstituted. Using UV footprinting, we show that the upstream AT-rich sequences of the murine IFN-␤ promoter constitute a preferential binding region for histone H1. Transfection with a plasmid carrying scaffold attachment regions as well as incubation with distamycin led to the derepression of the IFN-␤ promoter stably integrated into chromatin. In vitro, HMGI protein was able to displace histone H1 from the upstream AT-rich region of the wild-type promoter but not from the promoter carrying mutations on the upstream high-affinity HMGI binding site. Our results suggest that the binding of histone H1 to the upstream AT-rich region of the promoter might be partly responsible for the constitutive repression of the promoter. The displacement by HMGI protein of histone H1 could help to convert the IFN-␤ promoter from a repressed to an active state.

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Section: High-affinity Binding Of the Hmgi Protein To The Upstream Atmentioning

confidence: 99%

Specific Binding of High-Mobility-Group I (HMGI) Protein and Histone H1 to the Upstream AT-Rich Region of the Murine Beta Interferon Promoter: HMGI Protein Acts as a Potential Antirepressor of the Promoter

Bonnefoy

Bandu

Doly

1999

Molecular and Cellular Biology

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“…Linker histones are so called because of their role in keeping the nucleosomes juxtaposed, to form a highly compacted chromatin structure. Apart from their structural role, they participate in other regulatory functions, such as DNA repair (Downs et al, 2003), apoptosis (Konishi et al, 2003) and gene expression (Bouvet et al, 1994;Steinbach et al, 1997). Msx-1 targets H1b to the regulatory region of MyoD, and this recruitment is necessary for Msx-1 dependent repression of MyoD and inhibition of myogenesis (Lee et al, 2004).…”

Section: Stage 1-acquisition Of the Myogenic Lineagementioning

confidence: 99%

The epigenetic network regulating muscle development and regeneration

Palacios

Puri

2005

Journal Cellular Physiology

105

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This review focuses on our current knowledge of the epigenetic changes regulating gene expression at the chromatin and DNA level, independently on the primary DNA sequence, to reprogram the nuclei of muscle precursors during developmental myogenesis and muscle regeneration. These epigenetic marks provide the blueprint by which the extra-cellular cues are interpreted at the nuclear level by the transcription machinery to select the repertoire of tissue-specific genes to be expressed. The reversibility of some of these changes necessarily reflects the dynamic nature of skeletal myogenesis, which entails the progression through two antagonistic processes-proliferation and differentiation. Other epigenetic modifications are instead associated to events conventionally considered as irreversible-e.g. maintenance of lineage commitment and terminal differentiation. However, recent results support the possibility that these events can be reversed, at least upon certain experimental conditions, thereby revealing a dynamic nature of many of the epigenetic modifications underlying skeletal myogenesis. The elucidation of the epigenetic network that regulates transcription during developmental myogenesis and muscle regeneration might provide the information instrumental to devise pharmacological interventions toward selective manipulation of gene expression to promote regeneration of skeletal muscles and possibly other tissue.

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“…In Tetrahymena strains lacking the globular domain of histone H1, a subset of genes are activated or repressed (Shen and Gorovsky, 1996). During development in H1-de®cient Xenopus laevis, certain oocyte-speci®c 5S rRNA and mesodermal-speci®c genes are constitutively active (Bouvet et al, 1994;Steinback et al, 1997). Phosphorylation of H1 regulates its e ect on transcriptional activation, and occurs primarily on the basic N-and Cterminal tails (Wol e and Hayes, 1999).…”

Section: Gr and Histone H1 Phosphorylationmentioning

confidence: 99%

Glucocorticoid receptor-mediated chromatin remodeling in vivo

Deroo

Archer

2001

Oncogene

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The compaction of DNA into chromatin provides an additional level of gene regulation in eukaryotes that may not be available to prokaryotes. When packaged as chromatin, most promoters are transcriptionally repressed, and transcription factors have reduced access to their binding sites. The glucocorticoid receptor (GR) is a ligand-activated transcription factor that regulates the activity of genes involved in many physiological processes. To regulate eukaryotic genes, the GR binds to target sites within promoter regions of genes assembled as chromatin. This interaction alters the nucleosomal architecture to allow binding of other transcription factors, and formation of the preinitiation complex. The mouse mammary tumor virus (MMTV) promoter has been used extensively as a model to explore the processes by which the GR remodels chromatin and activates transcription. Signi®cant progress has been made in our understanding of the mechanisms used by the GR to modify chromatin structure, and the limits placed on the GR by post-translational modi®cations of histones. We will describe recent developments in the processes used by the GR to activate transcription in vivo via chromatin remodeling complexes, histone H1 phosphorylation, and recruitment of diverse coactivators. Oncogene (2001) 20, 3039 ± 3046.

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Specific regulation of Xenopus chromosomal 5S rRNA gene transcription in vivo by histone H1.

Cited by 233 publications

References 91 publications

Specific Binding of High-Mobility-Group I (HMGI) Protein and Histone H1 to the Upstream AT-Rich Region of the Murine Beta Interferon Promoter: HMGI Protein Acts as a Potential Antirepressor of the Promoter

Specific Binding of High-Mobility-Group I (HMGI) Protein and Histone H1 to the Upstream AT-Rich Region of the Murine Beta Interferon Promoter: HMGI Protein Acts as a Potential Antirepressor of the Promoter

The epigenetic network regulating muscle development and regeneration

Glucocorticoid receptor-mediated chromatin remodeling in vivo

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