Chromatin disruption and modification

Wolffe, Alan P.; Hayes, Jeffrey J.

doi:10.1093/nar/27.3.711

Cited by 501 publications

(345 citation statements)

References 173 publications

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“…Gene expression during long-term synaptic plasticity requires the activation of transcription factors, as well as chromatin remodeling (Wolffe and Hayes, 1999;Rosenfeld and Glass, 2001). As a regulator of gene expression, PARP-1 seems to play a critical role in both these processes.…”

Section: Discussionmentioning

confidence: 99%

Histone H1 Poly[ADP]-Ribosylation Regulates the Chromatin Alterations Required for Learning Consolidation

Fontán‐Lozano

Suárez-Pereira²,

Horrillo³

et al. 2010

J. Neurosci.

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Section: Discussionmentioning

confidence: 99%

Histone H1 Poly[ADP]-Ribosylation Regulates the Chromatin Alterations Required for Learning Consolidation

Fontán‐Lozano

Suárez-Pereira²,

Horrillo³

et al. 2010

J. Neurosci.

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“…Histone acetylation may decrease the stability of the compacted 30-nm chromatin fiber (36) and thereby destabilize the higher order structures through which chromatin is folded into the chromosome (37). Unfolding of chromatin may facilitate many nuclear processes (transcription, replication, recombination, methylation, and DNA repair) and be reflected in a variety of indirect assays and observations (accessibility to endonucleases, timing of replication, nuclear position, and patterns of DNA methylation).…”

Section: Discussionmentioning

confidence: 99%

Identification of a conserved erythroid specific domain of histone acetylation across the α-globin gene cluster

Anguita

Johnson

Wood

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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We have analyzed the pattern of core histone acetylation across 250 kb of the telomeric region of the short arm of human chromosome 16. This gene-dense region, which includes the ␣-globin genes and their regulatory elements embedded within widely expressed genes, shows marked differences in histone acetylation between erythroid and non-erythroid cells. In non-erythroid cells, there was a uniform 2-to 3-fold enrichment of acetylated histones, compared with heterochromatin, across the entire region. In erythroid cells, an Ϸ100-kb segment of chromatin encompassing the ␣ genes and their remote major regulatory element was highly enriched in histone H4 acetylated at Lys-5. Other lysines in the N-terminal tail of histone H4 showed intermediate and variable levels of enrichment. Similar broad segments of erythroid-specific histone acetylation were found in the corresponding syntenic regions containing the mouse and chicken ␣-globin gene clusters. The borders of these regions of acetylation are located in similar positions in all three species, and a sharply defined 3 boundary coincides with the previously identified breakpoint in conserved synteny between these species. We have therefore demonstrated that an erythroid-specific domain of acetylation has been conserved across several species, encompassing not only the ␣-globin genes but also a neighboring widely expressed gene. These results contrast with those at other clusters and demonstrate that not all genes are organized into discrete regulatory domains.A n important question in the postgenome era concerns the relationship between chromosome structure and function, in particular whether genes and the cis-acting sequences regulating their expression are organized into discrete chromosomal domains. To date, such domains have been variously defined by nuclease sensitivity, histone acetylation, replication timing, and DNA methylation (1). Specialized elements flanking such domains are thought to demarcate the transition between active and inactive chromatin and may isolate cis-acting elements within the domain from the influence of those outside (2-4). It has been suggested that some, but not all, boundary elements co-map with nuclear matrix attachment sites (3). Such independently regulated domains are proposed to be a regular feature of genome organization in eukaryotic chromosomes (2, 3).The human ␣-globin cluster provides a challenge to this model. The embryonic ( ) and fetal͞adult (␣) ␣-like genes lie within a gene dense region close to the telomere of the short arm of chromosome 16 (5). Although the and ␣ genes are expressed in a tissue-and developmental stage-specific manner, they are closely flanked by widely expressed genes. Curiously, their major regulatory element (␣MRE) lies 40 kb upstream of the -␣ cluster within the intron of a widely expressed gene (C16orf35) (6, 7). Clearly, this arrangement is not consistent with a model in which independently regulated genes are arranged into structurally discrete domains. Nevertheless, it does not rule out a more com...

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“…A protein-inaccessible chromatin structure is also directly linked to the acetylation status of core histones in the nucleosomes of gene promoters (6,7). Hypoacetylated histones are associated with transcriptionally inert regions of heterochromatin, whereas acetylated histones are associated with transcriptionally active regions of euchromatin (8)(9)(10). Recent reports have identified a mechanistic pathway of epigenetic silencing by cytosine methylation, histone hypoacetylation and chromatin condensation suggesting that these mechanisms act together to inactivate gene transcription (11,12).…”

Section: Introductionmentioning

confidence: 99%

Transcriptional repression of BRCA1 by aberrant cytosine methylation, histone hypoacetylation and chromatin condensation of the BRCA1 promoter

Rice¹

2000

Nucleic Acids Research

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BRCA1 expression is repressed by aberrant cytosine methylation in sporadic breast cancer. We hypothesized that aberrant cytosine methylation of the BRCA1 promoter was associated with the transcriptionally repressive effects of histone hypoacetylation and chromatin condensation. To address this question, we developed an in vitro model of study using normal cells and sporadic breast cancer cells with known levels of BRCA1 transcript to produce a 1.4 kb 5-methylcytosine map of the BRCA1 5′ CpG island. While all cell types were densely methylated upstream of -728 relative to BRCA1 transcription start, all normal and BRCA1 expressing cells were non-methylated downstream of -728 suggesting that this region contains the functional BRCA1 5′ regulatory region. In contrast, the non-BRCA1 expressing UACC3199 cells were completely methylated at all 75 CpGs. Chromatin immunoprecipitations showed that the UACC3199 cells were hypoacetylated at both histones H3 and H4 in the BRCA1 promoter compared to non-methylated BRCA1 expressing cells. The chromatin of the methylated UACC3199 BRCA1 promoter was inaccessible to DNA-protein interactions. These data indicate that the epigenetic effects of aberrant cytosine methylation, histone hypoacetylation and chromatin condensation act together in a discrete region of the BRCA1 5′ CpG island to repress BRCA1 transcription in sporadic breast cancer.

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Chromatin disruption and modification

Cited by 501 publications

References 173 publications

Histone H1 Poly[ADP]-Ribosylation Regulates the Chromatin Alterations Required for Learning Consolidation

Histone H1 Poly[ADP]-Ribosylation Regulates the Chromatin Alterations Required for Learning Consolidation

Identification of a conserved erythroid specific domain of histone acetylation across the α-globin gene cluster

Transcriptional repression of BRCA1 by aberrant cytosine methylation, histone hypoacetylation and chromatin condensation of the BRCA1 promoter

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