High-order chromatin structure and the epigenome in SAHFs

Chandra, Tamir; Narita, Masashi

doi:10.4161/nucl.23189

Cited by 60 publications

(49 citation statements)

References 38 publications

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“…This is consistent with previous data showing enrichment for heterochromatin marks on arrays of nucleosomes containing the canonical H3.1 (Loyola et al 2006). Moreover, these findings support the hypothesis that a spatial rearrangement of pre--existing heterochromatin upon senescence entry is the predominant mechanism of SAHF formation (Chandra et al 2012;Chandra and Narita 2013) (see also below). Beyond the typical SAHF formation, chromatin is further reorganized upon senescence.…”

Section: Introductionsupporting

confidence: 82%

“…4a). Thus, although this repressive mark is locally enriched at specific genes (Narita et al 2003), its highly static pattern strongly suggests a 3D repositioning of pre--existing marks to form SAHF, rather than formation and spreading of new heterochromatin in SAHF (Chandra and Narita 2013). Of note, H3K9me3 is also dispensable for SAHF formation in cells where the H3K9me3 demethylase JMJD2D is overexpressed (Chandra et al 2012).…”

Section: Dynamics Of Architectural Components Upon Sahf Formationmentioning

confidence: 99%

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Chromatin maintenance and dynamics in senescence: a spotlight on SAHF formation and the epigenome of senescent cells

Corpet

Stucki

2014

Chromosoma

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Senescence is a stable proliferation arrest characterized by profound changes in cellular morphology and metabolism as well as by extensive chromatin reorganization in the nucleus. One particular hallmark of chromatin changes during senescence is the formation of punctate DNA foci in DAPI-stained senescent cells that have been called senescence-associated heterochromatin foci (SAHF). While many advances have been made concerning our understanding of the effectors of senescence, how chromatin is reorganized and maintained in senescent cells has remained largely elusive. Because chromatin structure is inherently dynamic, senescent cells face the challenge of developing chromatin maintenance mechanisms in the absence of DNA replication in order to maintain the senescent phenotype. Here, we summarize and review recent findings shedding light on SAHF composition and formation via spatial repositioning of chromatin, with a specific focus on the role of lamin B1 for this process. In addition, we discuss the physiological implication of SAHF formation, the role of histone variants, and histone chaperones during senescence and also elaborate on the more general changes observed in the epigenome of the senescent cells.

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Section: Introductionsupporting

confidence: 82%

Section: Dynamics Of Architectural Components Upon Sahf Formationmentioning

confidence: 99%

Chromatin maintenance and dynamics in senescence: a spotlight on SAHF formation and the epigenome of senescent cells

Corpet

Stucki

2014

Chromosoma

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“…SAHFs are highly organized structures, where Lys9 trimethylation on histone H3 (H3K9me3; a constitutive heterochromatin marker) forms the core, which is surrounded by a layer of H3K27me3 (a facultative heterochromatin marker). These repressive layers are clearly separated from the outer transcriptionally active layer, supporting the idea that SAHF formation may contribute to gene expression profile stability for both active and repressive genes, although the direct relationship between SAHFs and gene regulation is still elusive (Chandra and Narita 2013). Despite the striking structural alteration in chromatin, the global landscapes of the repressive histone marks are highly static during SAHF formation, with only localized alterations in some genic regions, thus suggesting that SAHFs are formed through a spatial repositioning of repressively marked chromatin (Chandra et al 2012).…”

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confidence: 60%

Redistribution of the Lamin B1 genomic binding profile affects rearrangement of heterochromatic domains and SAHF formation during senescence

et al. 2013

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Senescence is a stress-responsive form of stable cell cycle exit. Senescent cells have a distinct gene expression profile, which is often accompanied by the spatial redistribution of heterochromatin into senescence-associated heterochromatic foci (SAHFs). Studying a key component of the nuclear lamina lamin B1 (LMNB1), we report dynamic alterations in its genomic profile and their implications for SAHF formation and gene regulation during senescence. Genome-wide mapping reveals that LMNB1 is depleted during senescence, preferentially from the central regions of lamina-associated domains (LADs), which are enriched for Lys9 trimethylation on histone H3 (H3K9me3). LMNB1 knockdown facilitates the spatial relocalization of perinuclear H3K9me3-positive heterochromatin, thus promoting SAHF formation, which could be inhibited by ectopic LMNB1 expression. Furthermore, despite the global reduction in LMNB1 protein levels, LMNB1 binding increases during senescence in a small subset of gene-rich regions where H3K27me3 also increases and gene expression becomes repressed. These results suggest that LMNB1 may contribute to senescence in at least two ways due to its uneven genome-wide redistribution: first, through the spatial reorganization of chromatin and, second, through gene repression.

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“…Acetylation of histones H3 and H4 is associated with "active" chromatin mark regions (Dawson and Kouzarides, 2012), whereas H3K27me3 and H3K9me3 are strongly correlated with silenced genes and considered to be repressive histone marks (Chandra and Narita, 2013). To determine whether IL-4 has a role in the alternation of chromatin structure, we purified histones from Ramos cells with the histone purification kit (Active Motif).…”

Section: The Expression Of Histone Modification In Ramos Cells Alterementioning

confidence: 99%

Histone H3k9 and H3k27 Acetylation Regulates IL‐4/STAT6‐Mediated Igε Transcription in B Lymphocytes

Wang

Duan

et al. 2015

The Anatomical Record

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IL-4 activates STAT6 and causes the subsequent up-regulation of Ig heavy chain germline Ige via chromatin remodeling involved in B lymphocytes development. STAT6 acts as a molecular switch to regulate the higher-order chromatin remodeling via dynamically orchestrating co-activators (CBP/Tudor-SN) and co-repressors (HDAC1/PSF). Here, we demonstrated that STAT6/Tudor-SN/PSF form a complex, balancing the acetylation and deacetylation states to co-regulate IL-4/STAT6 gene transcription. In addition, we confirmed that IL-4 treatment increased the HATs activity in Ramos cells. As "active" markers, the expression of H3K9ac and H3K27ac increased after treatment with IL-4. However, transcriptional repressors such as H3K9me3 and H3K27me3 decreased in response to IL-4 stimulation. Moreover, IL-4 treatment enhanced H3 acetylation at the Ige promoter regions. Our results revealed that the Ige gene transcription is regulated by histone modifications in the IL-4/STAT6 pathway. The study will provide novel insights into the pathogenesis of allergic diseases.

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High-order chromatin structure and the epigenome in SAHFs

Cited by 60 publications

References 38 publications

Chromatin maintenance and dynamics in senescence: a spotlight on SAHF formation and the epigenome of senescent cells

Chromatin maintenance and dynamics in senescence: a spotlight on SAHF formation and the epigenome of senescent cells

Redistribution of the Lamin B1 genomic binding profile affects rearrangement of heterochromatic domains and SAHF formation during senescence

Histone H3k9 and H3k27 Acetylation Regulates IL‐4/STAT6‐Mediated Igε Transcription in B Lymphocytes

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