Nucleosome assembly protein-1 (NAP-1) is regulator of histone H1 acetylation
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ABSTRACT:
PROVIDER: PRJNA668308 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12800917_1.fastq.gz | Fastqsanger.gz | |||
| SRR12800917_2.fastq.gz | Fastqsanger.gz | |||
| SRR12800918_1.fastq.gz | Fastqsanger.gz | |||
| SRR12800918_2.fastq.gz | Fastqsanger.gz | |||
| SRR12800919_1.fastq.gz | Fastqsanger.gz |
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Project description:We identified NAP-1 as regulator of histone H1 acetyation.
2020-10-10 | GSE159294 | GEO
Project description:Linker histones are involved in the formation of higher-order chromatin structure. Although linker histones have been implicated in the regulation of specific genes, it still remains unclear what their principal binding determinants are and how their repressive function in vitro can be reconciled with presumed broad binding in vivo. We generated a full genome, high resolution binding map of linker histone H1 in Drosophila Kc cells, using DamID. H1 binds at similar levels across much of the genome, both in classical euchromatin and heterochromatin. Strikingly, there are pronounced dips of low H1 occupancy around transcription start sites of active genes and at many distant cis-regulatory sites. H1 dips are not due to lack of nucleosomes. Rather, all regions with low binding of H1 show enrichment of the histone variant H3.3 which itself has been linked to high nucleosome turnover. Upon knockdown of H3.3, we find that H1 levels increase at sites previously not covered with H1 with a concomitant increase in nucleosome repeat length. These changes are independent of transcriptional changes. Our results show that the H3.3 protein counteracts association of H1 at genomic sites with high rates of histone turnover. This antagonism provides a mechanism to keep diverse genomic sites in an open chromatin conformation. For this study, we generated DamID profiles of histone H1 and RpII18 in Drosophila Kc167 cells. Additionally, we generated H1 profiles in cells treated with RNAi against white, H3.3B, or H3.3A and H3.3B. Nucleosome occupancy profiles were generated in untreated cells and cells treated with RNAi against white or H3.3A and H3.3B. Profiles of expression changes were generated for H3.3B RNAi and H3.3A and H3.3B RNAi.
2009-10-15 | GSE16882 | GEO
Project description:Linker histones are involved in the formation of higher-order chromatin structure. Although linker histones have been implicated in the regulation of specific genes, it still remains unclear what their principal binding determinants are and how their repressive function in vitro can be reconciled with presumed broad binding in vivo. We generated a full genome, high resolution binding map of linker histone H1 in Drosophila Kc cells, using DamID. H1 binds at similar levels across much of the genome, both in classical euchromatin and heterochromatin. Strikingly, there are pronounced dips of low H1 occupancy around transcription start sites of active genes and at many distant cis-regulatory sites. H1 dips are not due to lack of nucleosomes. Rather, all regions with low binding of H1 show enrichment of the histone variant H3.3 which itself has been linked to high nucleosome turnover. Upon knockdown of H3.3, we find that H1 levels increase at sites previously not covered with H1 with a concomitant increase in nucleosome repeat length. These changes are independent of transcriptional changes. Our results show that the H3.3 protein counteracts association of H1 at genomic sites with high rates of histone turnover. This antagonism provides a mechanism to keep diverse genomic sites in an open chromatin conformation. For this study, we generated DamID profiles of histone H1 and RpII18 in Drosophila Kc167 cells. Additionally, we generated H1 profiles in cells treated with RNAi against white, H3.3B, or H3.3A and H3.3B. Nucleosome occupancy profiles were generated in untreated cells and cells treated with RNAi against white or H3.3A and H3.3B. Profiles of expression changes were generated for H3.3B RNAi and H3.3A and H3.3B RNAi. DamID experiments for H1 and RpII18 were performed in Drosophila cell cultures. Samples were hybridized to 380k NimbleGen arrays with 300 bp probe spacing. Formaldehyde-assisted isolation of regulatotry elements (FAIRE) was performed in Drosophila Kc167 cells. Samples were hybridized to 380k NimbleGen arrays with 300 bp probe spacing over non-crosslinked genomic DNA. Nucleosome positioning profiles were made by hybridizing mononucleosomal DNA over MNase digested purified genomic DNA on 380k NimbleGen arrays with 10 bp probe spacing. Expression profiles were made as H3.3 RNAi over white RNAi cohybridizations on spotted INDAC long oligo arrays. Every experiment was done in duplicate in the reverse dye orientation.
2010-06-23 | E-GEOD-16882 | biostudies-arrayexpress
Project description:We identify acetylation of linker histone H1 lysine 85 as a novel histone acetylation mark, which regulates chromatin structure and genome stability upon DNA damage. By performing a chromatin immunoprecipitation and deep sequencing assay, we identified the genome-wide distribution patterns of H1 lysine 85 acetylation in HCT116 cells. We found that H1K85ac largely bound intergenic regions (53%) and gene bodies (39%), whereas only 7% H1K85ac bound regions 2 kb upstream of the transcription start sites (TSSs). As the proportion of H1K85ac bound to potential promoter regions was not significantly different to that of the random peaks (~6%), these data suggest that H1K85ac may not be mainly involved in general transcriptional regulation.
2018-04-18 | GSE113238 | GEO
Project description:The formation of accessible chromatin around DNA double-strand breaks is essential for their efficient repair1. Although the linker histone H1 is known to facilitate higher-order chromatin compaction2,3, the mechanisms by which H1 modifications regulate chromatin relaxation in response to DNA damage are unclear. Here we show that CTP synthase 1 (CTPS1)-catalysed deamidation of H1 asparagine residues 76 and 77 triggers the sequential acetylation of lysine 75 following DNA damage, and this dual modification of H1 is associated with chromatin opening. Mechanistically, the histone acetyltransferase p300 showed a preference for deamidated H1 as a substrate, establishing H1 deamidation as a prerequisite for subsequent acetylation. Moreover, high expression of CTPS1 was associated with resistance to cancer radiotherapy, in both mouse xenograft models and clinical cohorts. These findings provide new insights into how linker histones regulate dynamic chromatin alterations in the DNA damage response.
2025-02-03 | GSE288071 | GEO
Project description:NAP - neuroprotective peptide demonstrates increase in neuronal survival when injected into the hippocampus of rats in the model of epilepsy Microarray analysis was used to understand the expression of genes following KA treatment and the changes in gene expression following KA+NAP treatment Keywords: stress response KA was injected into the hippocampus of Sprague-Dawley rats. The other group of rats was injected with KA and NAP(10-13M). The third group was injected with NAP only and the last group was injected with PBS as a vehicle. CA3 area of hippocampus was removed 24h later and RNA extraction was done. The samples were subjected to microarray analysis.
2010-04-06 | E-GEOD-10923 | biostudies-arrayexpress
Project description:Linker histone H1 plays a key role in chromatin organization and maintenance, however, our knowledge of the regulation of H1 functions by its posttranslational modifications (PTMs) is very limited. In this study, we report on the generation of homogeneously and site-specifically mono- and di-acetylated H1 (H1 Ac) using genetic code expansion. We used these modified histones to identify and comprehensively characterize the acetylation-dependent cellular interactome for linker histone H1 and show that site-specific acetylation results in overlapping, but distinct groups of interacting partners. Intriguingly, H1 acetylation-specific interactors comprise translational initiation factors and are involved in transcriptional regulation, suggesting that acetylation of H1 may indeed act as a regulator of the linker histone H1 by modulation of protein-protein interactions.
2021-07-09 | PXD025832 | Pride
Project description:Histone H1 variants, known as linker histones, are essential chromatin components in higher eukaryotes, yet compared to the core histones relatively little is known about their in vivo functions. The filamentous fungus Neurospora crassa encodes a single H1 protein that is not essential for viability. To investigate the role of N. crassa H1, we constructed a functional FLAG-tagged H1 fusion protein and performed genomic and molecular analyses. Cell fractionation experiments showed that H1-FLAG is a chromatin binding protein. Chromatin-immunoprecipitation combined with sequencing (ChIP-seq) revealed that H1-3XFLAG is globally enriched throughout the genome with a subtle preference for promoters of expressed genes. In mammals, the stochiometery of H1 impacts nucleosome repeat length. To determine if H1 impacts nucleosome occupancy or nucleosome positioning in N. crassa, we performed micrococcal nuclease digestion in wildtype and the ∆hH1 strain followed by sequencing (MNase-Seq). Deletion of hH1 did not significantly impact nucleosome positioning or nucleosome occupancy. Analysis of DNA methylation using methylC-sequencing (mC-Seq) revealed a modest but global increase in DNA methylation in the ∆hH1 mutant. Together, these data suggest that H1 acts as a non-specific chromatin binding protein that can limit accessibility of the DNA methylation machinery in N. crassa.
2016-04-20 | GSE78157 | GEO
Project description:Drosophila dosage compensation is an epigenetic phenomenon in which the transcription of most genes on X-chromosome is enhanced by approximately two folds in males to equalize that in females. In this study, we provide evidence that transcriptional repressors, such as HP1 and linker histone H1, are globally reduced on male X chromosome. We further investigated the role of HP1 and linker H1 on X chromosome dosage compensation using flies with overexpression of HP1 and H1, we demonstrate that these repressors surpress H4K16 acetylation, presence of the elongating RNA Pol II and the transcription of the genes on male X chromosomes. To understand how H1 and HP1 are regulated on male X chromosome, we next explored the relationship between MOF and the two repressors of chromatin. We show that the hyperacetylation of H4K16 induced by MOF resulted in the loss of H1 and HP1 on chromatin and global chromatin decondensation. Our biochemical analysis further shows that the presence of acetylation on histone H4 at lysine 16 directly inhibits the interaction between histone H4 and linker H1. This study therefore provides novel clues on understanding the dynamic regulation of chromatin regulators on male X chromosome dosage compensation.
2017-11-01 | GSE29537 | GEO
Project description:NAP - neuroprotective peptide demonstrates increase in neuronal survival when injected into the hippocampus of rats in the model of epilepsy Microarray analysis was used to understand the expression of genes following KA treatment and the changes in gene expression following KA+NAP treatment Keywords: stress response
2010-03-01 | GSE10923 | GEO