NRP histone chaperones promote the removal of histone variant H2A.Z
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA525997 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10502946.fastq.gz | Fastqsanger.gz | |||
| SRR10502947.fastq.gz | Fastqsanger.gz | |||
| SRR10502948.fastq.gz | Fastqsanger.gz | |||
| SRR10502949.fastq.gz | Fastqsanger.gz | |||
| SRR10502950.fastq.gz | Fastqsanger.gz |
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Project description:In eukaryotes, DNA wraps around histones to form nucleosomes, which are compacted into chromatin. DNA-templated processes, including transcription, require chromatin disassembly and reassembly mediated by histone chaperones. Additionally, distinct histone variants can replace core histones to regulate chromatin structure and function. Although replacement of H2A with the evolutionarily conserved H2A.Z via the SWR1 histone chaperone complex has been extensively studied, in plants little is known about how a reduction of H2A.Z levels can be achieved in plants. Here, we show that NRP proteins cause a decrease of H2A.Z-containing nucleosomes in Arabidopsis under standard growing conditions. nrp1-1 nrp2-2 double mutants show an over-accumulation of H2A.Z genome-wide, especially at heterochromatic regions normally H2A.Z-depleted in wild-type plants. Our work suggests that NRP proteins regulate gene expression by counteracting SWR1, thereby preventing excessive accumulation of H2A.Z.
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Project description:The aim of this study was to uncover cell cycle dependent chromatin binding of H2A.Z and its histone chaperones. U2OS cells were stably transfected with Twin-Strep-tagged H2A.Z, ANP32e, or YL1 constructs, and WT cells were used as a negative/background control. U2OS cells were synchronised in G1 or G2-M phase using hydroxyurea or nocodazole, respectively, and protein-DNA complexes were isolated by affinity purification.
2023-06-29 | E-MTAB-11617 | biostudies-arrayexpress
Project description:In eukaryotes, DNA wraps around histones to form nucleosomes, which are compacted into chromatin. DNA-templated processes, including transcription, require chromatin disassembly and reassembly mediated by histone chaperones. Additionally, distinct histone variants can replace core histones to regulate chromatin structure and function. Although replacement of H2A with the evolutionarily conserved H2A.Z via the SWR1 histone chaperone complex has been extensively studied, in plants little is known about how a reduction of H2A.Z levels can be achieved. Here, we show that NRP proteins cause a decrease of H2A.Z-containing nucleosomes in Arabidopsis under standard growing conditions. nrp1-1 nrp2-2 double mutants show an over-accumulation of H2A.Z genome-wide, especially at heterochromatic regions normally H2A.Z-depleted in wild-type plants. Our work suggests that NRP proteins regulate gene expression by counteracting SWR1, thereby preventing excessive accumulation of H2A.Z.
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Project description:ChIP-seq of H2A.Z and its histone chaperones during the cell cycle
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Project description:Plants can sense temperature changes and adjust their development and morphology accordingly in a process called thermomorphogenesis. This phenotypic plasticity implies complex mechanisms regulating gene expression reprogramming in response to environmental alteration. Histone variants contribute to the chromatin dynamics and transcriptional control, yet how their deposition/eviction modulates transcriptional changes induced by environmental cues remains elusive. In Arabidopsis thaliana, temperature elevation-induced transcriptional activation at thermo-responsive genes entails the chromatin eviction of a histone variant H2A.Z by INO80, which is recruited to these loci via interacting with a key thermomorphogenesis regulator PHYTOCHROME-INTERACTING FACTOR 4 (PIF4). Here, we show that both INO80 and the deposition chaperones of another histone variant H3.3 associate with EARLY FLOWERING7 (ELF7), a critical component of the transcription elongation factor polymerase-associated factor 1 complex (PAF1c). H3.3 promotes thermomorphogenesis and the high temperature-enhanced RNA Pol II transcription at PIF4 targets, and it is broadly required for the H2A.Z removal-induced gene activation. Reciprocally, INO80 and ELF7 regulate H3.3 deposition, and are necessary for the high temperature-induced H3.3 enrichment at PIF4 targets. Our findings demonstrate close coordination between H2A.Z eviction and H3.3 deposition in gene activation induced by high temperature, and pinpoint the importance of histone variants dynamics in transcriptional regulation.
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Project description:Plants can sense temperature changes and adjust their development and morphology accordingly in a process called thermomorphogenesis. This phenotypic plasticity implies complex mechanisms regulating gene expression reprogramming in response to environmental alteration. Histone variants contribute to the chromatin dynamics and transcriptional control, yet how their deposition/eviction modulates transcriptional changes induced by environmental cues remains elusive. In Arabidopsis thaliana, temperature elevation-induced transcriptional activation at thermo-responsive genes entails the chromatin eviction of a histone variant H2A.Z by INO80, which is recruited to these loci via interacting with a key thermomorphogenesis regulator PHYTOCHROME-INTERACTING FACTOR 4 (PIF4). Here, we show that both INO80 and the deposition chaperones of another histone variant H3.3 associate with EARLY FLOWERING7 (ELF7), a critical component of the transcription elongation factor polymerase-associated factor 1 complex (PAF1c). H3.3 promotes thermomorphogenesis and the high temperature-enhanced RNA Pol II transcription at PIF4 targets, and it is broadly required for the H2A.Z removal-induced gene activation. Reciprocally, INO80 and ELF7 regulate H3.3 deposition, and are necessary for the high temperature-induced H3.3 enrichment at PIF4 targets. Our findings demonstrate close coordination between H2A.Z eviction and H3.3 deposition in gene activation induced by high temperature, and pinpoint the importance of histone variants dynamics in transcriptional regulation.
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Project description:Plants can sense temperature changes and adjust their development and morphology accordingly in a process called thermomorphogenesis. This phenotypic plasticity implies complex mechanisms regulating gene expression reprogramming in response to environmental alteration. Histone variants contribute to the chromatin dynamics and transcriptional control, yet how their deposition/eviction modulates transcriptional changes induced by environmental cues remains elusive. In Arabidopsis thaliana, temperature elevation-induced transcriptional activation at thermo-responsive genes entails the chromatin eviction of a histone variant H2A.Z by INO80, which is recruited to these loci via interacting with a key thermomorphogenesis regulator PHYTOCHROME-INTERACTING FACTOR 4 (PIF4). Here, we show that both INO80 and the deposition chaperones of another histone variant H3.3 associate with EARLY FLOWERING7 (ELF7), a critical component of the transcription elongation factor polymerase-associated factor 1 complex (PAF1c). H3.3 promotes thermomorphogenesis and the high temperature-enhanced RNA Pol II transcription at PIF4 targets, and it is broadly required for the H2A.Z removal-induced gene activation. Reciprocally, INO80 and ELF7 regulate H3.3 deposition, and are necessary for the high temperature-induced H3.3 enrichment at PIF4 targets. Our findings demonstrate close coordination between H2A.Z eviction and H3.3 deposition in gene activation induced by high temperature, and pinpoint the importance of histone variants dynamics in transcriptional regulation.
2023-01-13 | GSE221657 | GEO
Project description:Plants can sense temperature changes and adjust their development and morphology accordingly in a process called thermomorphogenesis. This phenotypic plasticity implies complex mechanisms regulating gene expression reprogramming in response to environmental alteration. Histone variants contribute to the chromatin dynamics and transcriptional control, yet how their deposition/eviction modulates transcriptional changes induced by environmental cues remains elusive. In Arabidopsis thaliana, temperature elevation-induced transcriptional activation at thermo-responsive genes entails the chromatin eviction of a histone variant H2A.Z by INO80, which is recruited to these loci via interacting with a key thermomorphogenesis regulator PHYTOCHROME-INTERACTING FACTOR 4 (PIF4). Here, we show that both INO80 and the deposition chaperones of another histone variant H3.3 associate with EARLY FLOWERING7 (ELF7), a critical component of the transcription elongation factor polymerase-associated factor 1 complex (PAF1c). H3.3 promotes thermomorphogenesis and the high temperature-enhanced RNA Pol II transcription at PIF4 targets, and it is broadly required for the H2A.Z removal-induced gene activation. Reciprocally, INO80 and ELF7 regulate H3.3 deposition, and are necessary for the high temperature-induced H3.3 enrichment at PIF4 targets. Our findings demonstrate close coordination between H2A.Z eviction and H3.3 deposition in gene activation induced by high temperature, and pinpoint the importance of histone variants dynamics in transcriptional regulation.
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2022-02-15 | PXD029061 | Pride
Project description:The regulation of eukaryotic chromatin relies on interactions between many epigenetic factors, including histone modifications, DNA methylation, and the incorporation of histone variants. H2A.Z, one of the most conserved but enigmatic histone variants that is enriched at the transcriptional start sites of genes, has been implicated in a variety of chromosomal processes. Recently, we reported a genome-wide anticorrelation between H2A.Z and DNA methylation, an epigenetic hallmark of heterochromatin that has also been found in the bodies of active genes in plants and animals. Here, we investigate the basis of this anticorrelation using a novel h2a.z loss-of-function line in Arabidopsis thaliana. Through genome-wide bisulfite sequencing, we demonstrate that a loss of H2A.Z in Arabidopsis does not affect the level or profile of DNA methylation in genes, and we propose that the global anticorrelation between DNA methylation and H2A.Z is caused by the exclusion of H2A.Z from methylated DNA. RNA-seq and genomic mapping of H2A.Z show that H2A.Z enrichment across gene bodies, rather than at the TSS, is correlated with lower transcription levels and higher measures of gene responsiveness. We find that a loss of H2A.Z causes misregulation of many genes that are disproportionately associated with response to both endogenous and exogenous stimuli. We propose that H2A.Z deposition in gene bodies promotes variability in levels and patterns of gene expression, and that a major function of genic DNA methylation is to exclude H2A.Z from constitutively expressed genes. Examination of DNA methylation and transcription in an h2a.z mutant
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