Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Age and cell type specific specific effects of histone variant H2BE in the brain [RNASeq]

ABSTRACT: Transcription is regulated in part through histone proteins that complex with DNA and control access to genes. Histones can be replaced with variant forms that are particularly critical in the brain and accumulate throughout lifespan. Recently, we defined the first broadly expressed H2B variant, H2BE, and demonstrated that it regulates chromatin structure, neuronal transcription, and mouse behavior. However, the role of H2BE in other cell types and its role throughout lifespan remain unknown. Here, we discovered that H2BE is highly expressed in astrocytes as well as neurons and accumulates with age in both cell types. Using single-nucleus RNA-sequencing, we demonstrate that loss of H2BE robustly affects gene expression in both astrocytes and neurons, with divergent effects in young and aging brains. Interestingly, loss of H2BE in young brains causes similar gene expression changes as aging and some effects of aging are reversed with H2BE loss. Lastly, behavioral testing demonstrates that H2BE loss disrupts long-term memory but improves working memory in aging mice. Together, these data provide novel links between histone variants, aging-related gene expression changes in both astrocytes and neurons, and memory.

ORGANISM(S): Mus musculus

PROVIDER: GSE282468 | GEO | 2025/11/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Age and cell type specific specific effects of histone variant H2BE in the brain [Intact_RNAseq]

Project description:Transcription is regulated in part through histone proteins that complex with DNA and control access to genes. Histones can be replaced with variant forms that are particularly critical in the brain and accumulate throughout lifespan. Recently, we defined the first broadly expressed H2B variant, H2BE, and demonstrated that it regulates chromatin structure, neuronal transcription, and mouse behavior. However, the role of H2BE in other cell types and its role throughout lifespan remain unknown. Here, we discovered that H2BE is highly expressed in astrocytes as well as neurons and accumulates with age in both cell types. Using single-nucleus RNA-sequencing, we demonstrate that loss of H2BE robustly affects gene expression in both astrocytes and neurons, with divergent effects in young and aging brains. Interestingly, loss of H2BE in young brains causes similar gene expression changes as aging and some effects of aging are reversed with H2BE loss. Lastly, behavioral testing demonstrates that H2BE loss disrupts long-term memory but improves working memory in aging mice. Together, these data provide novel links between histone variants, aging-related gene expression changes in both astrocytes and neurons, and memory.

2025-11-13 | GSE282467 | GEO

Age and cell type specific specific effects of histone variant H2BE in the brain [ATACSeq]

2025-11-13 | GSE282469 | GEO

Age and cell type specific specific effects of histone variant H2BE in the brain [Cut&Tag]

2025-11-13 | GSE282519 | GEO

Age and cell type specific specific effects of histone variant H2BE in the brain [E2F_CUT&Tag]

2025-11-13 | GSE300097 | GEO

Age and cell type specific specific effects of histone variant H2BE in the brain [snRNA-seq]

2025-11-13 | GSE282520 | GEO

Age and cell type specific specific effects of histone variant H2BE in the brain [Cortex_CUT&Tag]

2025-11-13 | GSE300096 | GEO

Age- and cell type- specific effects of histone variant H2BE in the brain

Project description:Transcription is regulated in part through histone proteins that bind DNA and control access to genes. Histones can be replaced with variant forms that are particularly critical in the brain and accumulate throughout lifespan. Recent findings defined the first broadly expressed H2B variant, H2BE, and demonstrated that it regulates chromatin structure, neuronal transcription, and mouse behavior. However, the role of H2BE in other cell types and its role throughout lifespan remain unknown. Here, we discovered that H2BE is enriched in astrocytes in the brain and accumulates with age in both astrocytes and neurons. Using single-nucleus RNA-sequencing, we demonstrate that H2BE promotes synaptic gene expression in neurons and astrocytes in young brains. Using microelectrode array recordings, we discovered that H2BE is required in both cell types for proper synaptic function. In aging brains, loss of H2BE similarly affects synaptic genes in neurons but also dampens some age-related transcriptional changes in both astrocytes and neurons. Lastly, behavioral testing demonstrates that H2BE loss disrupts long-term memory but improves working memory in aging mice. Together, these data provide novel links between histone variants, aging-related gene expression changes in both astrocytes and neurons, and memory.

2025-11-09 | PXD069021 | panorama

Effects of H2be loss of function on gene expression in the main olfactory epithelium (MOE) of 6-month old mice.

Project description:We have identified a replication-independent histone variant, Hist2h2be (referred to herein as H2be), which is expressed exclusively by olfactory chemosensory neurons. Levels of H2BE are heterogeneous among olfactory neurons, but stereotyped according to the identity of the co-expressed olfactory receptor (OR). Gain- and loss-of-function experiments demonstrate that changes in H2be expression affect olfactory function and OR representation in the adult olfactory epithelium. We show that H2BE expression is reduced by sensory activity and that it promotes neuronal cell death, such that inactive olfactory neurons display higher levels of the variant and shorter life spans. Post-translational modifications (PTMs) of H2BE differ from those of the canonical H2B, consistent with a role for H2BE in altering transcription. We propose a physiological function for H2be in modulating olfactory neuron population dynamics to adapt the OR repertoire to the environment. The objective of generating this dataset was to analyze the effects of H2be loss of function on gene expression in the main olfactory epithelium of 6-month old mice. This dataset compares gene expression in wild type and H2be-KO main olfactory epithelium (MOE) samples. There are six replicates for each genotype (equal mixture of males and females).

2012-09-01 | E-GEOD-39515 | biostudies-arrayexpress

Genome-wide location analysis of FLAG-H2BE

Project description:We have identified a replication-independent histone variant, Hist2h2be (referred to herein as H2be), which is expressed exclusively by olfactory chemosensory neurons. Levels of H2BE are heterogeneous among olfactory neurons, but stereotyped according to the identity of the co-expressed olfactory receptor (OR). Gain- and loss-of-function experiments demonstrate that changes in H2be expression affect olfactory function and OR representation in the adult olfactory epithelium. We show that H2BE expression is reduced by sensory activity and that it promotes neuronal cell death, such that inactive olfactory neurons display higher levels of the variant and shorter life spans. Post-translational modifications (PTMs) of H2BE differ from those of the canonical H2B, consistent with a role for H2BE in altering transcription. We propose a physiological function for H2be in modulating olfactory neuron population dynamics to adapt the OR repertoire to the environment. The objective of generating this dataset was to analyze the occupancy of H2BE protein in the vicinity of gene promoters throughout the genome, relative to histone H3, in olfactory sensory neurons within the main olfactory epithelium (MOE). This dataset analyzes the occupancy of FLAG-H2BE protein in the vicinity of gene promoters throughout the genome, relative to histone H3, in olfactory sensory neurons within the main olfactory epithelium (MOE) of Flag-H2be transgenic mice, which express a FLAG-tagged version of H2BE from the H2be promoter. There are 2 replicates for each ChIP (FLAG and H3).

2012-09-01 | E-GEOD-39517 | biostudies-arrayexpress

Effects of H2be loss of function on gene expression changes in the main olfactory epithelium (MOE) as a result of activity deprivation through unilateral naris occlusion (UNO).

Project description:We have identified a replication-independent histone variant, Hist2h2be (referred to herein as H2be), which is expressed exclusively by olfactory chemosensory neurons. Levels of H2BE are heterogeneous among olfactory neurons, but stereotyped according to the identity of the co-expressed olfactory receptor (OR). Gain- and loss-of-function experiments demonstrate that changes in H2be expression affect olfactory function and OR representation in the adult olfactory epithelium. We show that H2BE expression is reduced by sensory activity and that it promotes neuronal cell death, such that inactive olfactory neurons display higher levels of the variant and shorter life spans. Post-translational modifications (PTMs) of H2BE differ from those of the canonical H2B, consistent with a role for H2BE in altering transcription. We propose a physiological function for H2be in modulating olfactory neuron population dynamics to adapt the OR repertoire to the environment. The objective of generating this dataset was to analyze the effects of H2be loss of function on gene expression changes in the main olfactory epithelium as a result of activity deprivation through unilateral naris occlusion (UNO). This dataset compares gene expression in wild type and H2be-KO main olfactory epithelium (MOE) samples from 5-week old mice that were subjected to unilateral naris occlusion (UNO) for 3 weeks starting from 2 weeks of age. Samples consist of MOE halves that were dissected and carefully removed from the medial bone. Each sample contains tissue from 2 mice (1 female and 1 male). There are three replicates for each genotype (H2be-KO or WT) and UNO side (open or closed) combination.

2012-09-01 | E-GEOD-39516 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data