Similar Datasets
Project description:Single-nucleus Drop-seq was used to profile transcriptional changes upon loss of H2BE in nuclei isolated from the cortex of young adult mice
2024-07-17 | GSE247340 | GEO
Project description:RNA-seq analysis of WT and H2BE-KO primary cortical neurons
| PRJNA1034131 | ENA
Project description:Histone variant H2BE Analysis of histone variant H2BE in neuronal chromatin
2024-07-17 | GSE246618 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE39514: Effects of H2be ectopic over-expression on gene expression in the main olfactory epithelium (MOE) of 5-week old mice. GSE39515: Effects of H2be loss of function on gene expression in the main olfactory epithelium (MOE) of 6-month old mice. GSE39516: 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). GSE39517: Genome-wide location analysis of FLAG-H2BE Refer to individual Series
2012-09-01 | E-GEOD-39674 | biostudies-arrayexpress
Project description:Analysis of histone variant H2BE in neuronal chromatin
2024-07-17 | GSE246748 | GEO
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
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).
2012-09-01 | GSE39517 | GEO
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
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 | GSE282468 | GEO
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