ATAD2 maintains the equilibrium between nucleosome assembly and disassembly
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA739885 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14877300_1.fastq.gz | Fastqsanger.gz | |||
| SRR14877300_2.fastq.gz | Fastqsanger.gz | |||
| SRR14877301_1.fastq.gz | Fastqsanger.gz | |||
| SRR14877301_2.fastq.gz | Fastqsanger.gz | |||
| SRR14877302_1.fastq.gz | Fastqsanger.gz |
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Project description:To avoid toxic histone overload, histone deposition and removal must be finely tuned. Following a series of functional studies in human, mouse and S. pombe, we show here that the AAA ATPase ATAD2 is a conserved mediator of histone removal and a regulator of histone deposition. In Atad2 knockout (KO) spermatogenic cells, the late-stage genome-wide eviction of histones and their replacement by protamines are significantly delayed. In S. pombe, deletion of abo1 leads to a dramatic decrease in cell growth, with the appearance of suppressor clones recovering normal growth. Identification of the corresponding suppressor mutations revealed that the causes of cell toxicity are mainly the deregulated activity of the histone chaperone HIRA and histone overload. We also show that, in Atad2 KO mouse ES cells, HIRA and FACT are trapped on nucleosomes at transcription start sites of active genes, resulting in histone overload and abnormal histone deposition on nucleosome-free regions. Overall, these data shed new light on a need for energy-consuming auxiliary factors, such as ATAD2, to maintain a balanced and dynamic histone chaperone basal activity and to avoid a deleterious histone overload.
2021-09-24 | GSE178647 | GEO
Project description:Chromatin remodeling factors and histone chaperones were previously shown to cooperatively affect nucleosome assembly and disassembly processes in vitro. Here we show that S. pombe CHD remodellers, Hrp1 and Hrp3 physically interact with the histone chaperone Nap1. Genome wide analysis of Hrp1, Hrp3 and Nap1 occupancy, combined with nucleosome density measurements in respective mutants revealed that the CHD factors and Nap1 co-localized in particular to promoter regions where they remove nucleosomes near the transcriptional start site. Hrp1 and Hrp3 also regulate nucleosome density in coding regions where they have redundant roles to stimulate transcription. Previously, DNA replication dependent and independent nucleosome disassembly processes have been described. We found that nucleosome density increased in the hrp1 mutant in the absence of DNA replication. Finally, regions where nucleosome density increased in hrp1, hrp3 and nap1 mutants also showed nucleosome density and histone modification changes in HDAC and HAT mutants. Thus, this study revealed an important in vivo role for CHD remodellers and Nap1 in nucleosome disassembly at promoters and coding regions, which are linked to changes in histone acetylation. Keywords: ChIP on CHIP and expression profiling
2007-05-19 | GSE6557 | GEO
Project description:Although the conserved AAA ATPase â bromodomain factor, ATAD2, has been described as a transcriptional co-activator upregulated in many cancers, its function remains poorly understood. Here, using a combination of ChIP-seq, ChIP-proteomics and RNA-seq experiments in embryonic stem cells, we found that Atad2 is an abundant nucleosome-bound protein present on active genes, associated with chromatin remodelling, DNA replication and DNA repair factors. A structural analysis of its bromodomain and subsequent investigations demonstrate that histone acetylation guides ATAD2 to chromatin, resulting in an overall increase of chromatin accessibility and histone dynamics, which is required for the proper activity of the highly expressed gene fraction of the genome. While in exponentially growing cells Atad2 appears dispensable for cell growth, in differentiating ES cells, Atad2 becomes critical in sustaining specific gene expression programs, controlling proliferation and differentiation. Altogether, this work defines Atad2âs function as a facilitator of general chromatin-templated activities such as transcription. Transcriptomic analyses comparing ES cells stably expressing anti-Atad2 shRNA versus cells expressing control shRNA, in day 3 LIF (-) differentiating ES cells (3 replicates for each condition) were performed using the Illumina MouseWG-6 v2.0 expression beadchip technology
2016-03-24 | E-GEOD-69899 | biostudies-arrayexpress
Project description:Although the conserved AAA ATPase – bromodomain factor, ATAD2, has been described as a transcriptional co-activator upregulated in many cancers, its function remains poorly understood. Here, using a combination of ChIP-seq, ChIP-proteomics and RNA-seq experiments in embryonic stem cells, we found that Atad2 is an abundant nucleosome-bound protein present on active genes, associated with chromatin remodelling, DNA replication and DNA repair factors. A structural analysis of its bromodomain and subsequent investigations demonstrate that histone acetylation guides ATAD2 to chromatin, resulting in an overall increase of chromatin accessibility and histone dynamics, which is required for the proper activity of the highly expressed gene fraction of the genome. While in exponentially growing cells Atad2 appears dispensable for cell growth, in differentiating ES cells, Atad2 becomes critical in sustaining specific gene expression programs, controlling proliferation and differentiation. Altogether, this work defines Atad2’s function as a facilitator of general chromatin-templated activities such as transcription.
2016-03-24 | GSE70314 | GEO
Project description:Although the conserved AAA ATPase – bromodomain factor, ATAD2, has been described as a transcriptional co-activator upregulated in many cancers, its function remains poorly understood. Here, using a combination of ChIP-seq, ChIP-proteomics and RNA-seq experiments in embryonic stem cells, we found that Atad2 is an abundant nucleosome-bound protein present on active genes, associated with chromatin remodelling, DNA replication and DNA repair factors. A structural analysis of its bromodomain and subsequent investigations demonstrate that histone acetylation guides ATAD2 to chromatin, resulting in an overall increase of chromatin accessibility and histone dynamics, which is required for the proper activity of the highly expressed gene fraction of the genome. While in exponentially growing cells Atad2 appears dispensable for cell growth, in differentiating ES cells, Atad2 becomes critical in sustaining specific gene expression programs, controlling proliferation and differentiation. Altogether, this work defines Atad2’s function as a facilitator of general chromatin-templated activities such as transcription.
2016-03-24 | GSE70313 | GEO
Project description:Although the conserved AAA ATPase – bromodomain factor, ATAD2, has been described as a transcriptional co-activator upregulated in many cancers, its function remains poorly understood. Here, using a combination of ChIP-seq, ChIP-proteomics and RNA-seq experiments in embryonic stem cells, we found that Atad2 is an abundant nucleosome-bound protein present on active genes, associated with chromatin remodelling, DNA replication and DNA repair factors. A structural analysis of its bromodomain and subsequent investigations demonstrate that histone acetylation guides ATAD2 to chromatin, resulting in an overall increase of chromatin accessibility and histone dynamics, which is required for the proper activity of the highly expressed gene fraction of the genome. While in exponentially growing cells Atad2 appears dispensable for cell growth, in differentiating ES cells, Atad2 becomes critical in sustaining specific gene expression programs, controlling proliferation and differentiation. Altogether, this work defines Atad2’s function as a facilitator of general chromatin-templated activities such as transcription.
2016-03-24 | GSE70312 | GEO
Project description:Although the conserved AAA ATPase – bromodomain factor, ATAD2, has been described as a transcriptional co-activator upregulated in many cancers, its function remains poorly understood. Here, using a combination of ChIP-seq, ChIP-proteomics and RNA-seq experiments in embryonic stem cells, we found that Atad2 is an abundant nucleosome-bound protein present on active genes, associated with chromatin remodelling, DNA replication and DNA repair factors. A structural analysis of its bromodomain and subsequent investigations demonstrate that histone acetylation guides ATAD2 to chromatin, resulting in an overall increase of chromatin accessibility and histone dynamics, which is required for the proper activity of the highly expressed gene fraction of the genome. While in exponentially growing cells Atad2 appears dispensable for cell growth, in differentiating ES cells, Atad2 becomes critical in sustaining specific gene expression programs, controlling proliferation and differentiation. Altogether, this work defines Atad2’s function as a facilitator of general chromatin-templated activities such as transcription.
2016-03-24 | GSE69899 | GEO
Project description:ATAD2, expressed predominantly in embryonic stem cells as well as in spermatogenic cells emerges as a pivotal regulator of chromatin dynamics by mediating chromatin-bound histone chaperone turnover. Here, investigating the role of ATAD2 in spermatogenesis, we show that through its preponderant expression in haploid male germ cells, ATAD2 modulates the HIRA-dependent H3.3 genome localization and H3.3-dependent gene transcriptional regulation. Furthermore, by influencing histone eviction and the assembly of protamines, it ensures proper chromatin condensation and genome packaging in mature spermatozoa. The disruption of Atad2 results in aberrant mature spermatozoa genome organization, impacting male fertility. Collectively, these findings confirm the occurrence of an overlooked chromatin dynamic regulatory level controlling histone deposition-removal balance, depending on an ATAD2-controlled histone chaperone-chromatin interaction.
2026-01-05 | GSE277943 | GEO
Project description:ATAD2, expressed predominantly in embryonic stem cells as well as in spermatogenic cells emerges as a pivotal regulator of chromatin dynamics by mediating chromatin-bound histone chaperone turnover. Here, investigating the role of ATAD2 in spermatogenesis, we show that through its preponderant expression in haploid male germ cells, ATAD2 modulates the HIRA-dependent H3.3 genome localization and H3.3-dependent gene transcriptional regulation. Furthermore, by influencing histone eviction and the assembly of protamines, it ensures proper chromatin condensation and genome packaging in mature spermatozoa. The disruption of Atad2 results in aberrant mature spermatozoa genome organization, impacting male fertility. Collectively, these findings confirm the occurrence of an overlooked chromatin dynamic regulatory level controlling histone deposition-removal balance, depending on an ATAD2-controlled histone chaperone-chromatin interaction.
2026-01-05 | GSE283879 | GEO
Project description:ATPase Family AAA domain containing 2 (ATAD2) expression is elevated in many cancer types including ovarian cancer. Therefore, we analyzed the role of ATAD2 in ovarian cancer. Pharmacological inhibition of ATAD2 expression in ovarian cancer cell lines resulted in decreased proliferation, and increased cell death.
2024-12-01 | GSE192673 | GEO