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Mapping the epigenomic and transcriptomic interplay during memory formation and recall in the hippocampal engram ensemble

ABSTRACT: Purpose: we utilized a mouse model that permanently labels neurons activated throughout a specific experience to decipher the interplay between chromatin accessibility, 3D-chromatin architecture and transcriptional changes across different memory phases. Non activated (basal) and activated neurons during memory encoding (early), consolidation (late) and recall (reactivated) were sorted and subjected to nuclear RNA sequencing (nRNA-seq) to determine gene expression, ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) to assess chromatin accessibility, chromosome conformation capture (Hi-C) to identify global 3D -genome architecture and promoter capture Hi-C to identify the long range promoter-enhancer interactions. Results: We have found that during each memory phase, the same promoters interact more frequently with a distinct subset of enhancers (i.e. unique). We also identified a smaller subset of interactions in which the promoters were interacting with the same enhancers across different memory phases (i.e. common). Furthermore, Reactivated neurons presented significantly stronger interaction scores (as calculated by CHiCAGO). Hence, although the number of unique interactions was similar across early, late and reactivated states, stronger interaction scores indicate that specific promoter- enhancer interactions occur more frequently during memory recall.

ORGANISM(S): Mus musculus

PROVIDER: GSE152955 | GEO | 2020/06/23

REPOSITORIES: GEO

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Mapping the epigenomic and transcriptomic interplay during memory formation and recall in the hippocampal engram ensemble

2020-06-23 | GSE152954 | GEO

Mapping the epigenomic and transcriptomic interplay during memory formation and recall in the hippocampal engram ensemble

Project description:Purpose: we utilized a mouse model that permanently labels neurons activated throughout a specific experience to decipher the interplay between chromatin accessibility, 3D-chromatin architecture and transcriptional changes across different memory phases. Non activated (basal) and activated neurons during memory encoding (early), consolidation (late) and recall (reactivated) were sorted and subjected to nuclear RNA sequencing (nRNA-seq) to determine gene expression, ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) to assess chromatin accessibility, chromosome conformation capture (Hi-C) to identify global 3D -genome architecture and promoter capture Hi-C to identify the long range promoter-enhancer interactions. Results: Our differentially expressed gene (DEG) analysis revealed relatively low amount of changes in the early phase, when compared to basal-state neurons (Basal vs. Early). In contrast, neurons from late phase presented higher numbers of DEGs despite there being more similarity in chromatin accessibility at these time points (Early vs. Late; Late vs. Reactivated). Our studies illuminate for the first time the unique transcriptional landscape of reactivated engram cells where we observed up-regulation of genes involved in mRNA transport and local protein translation in synaptic compartments. These changes corresponded to morphological and functional changes in those neurons.

2020-06-23 | GSE152775 | GEO

Mapping the epigenomic and transcriptomic interplay during memory formation and recall in the hippocampal engram ensemble

Project description:Purpose: we utilized a mouse model that permanently labels neurons activated throughout a specific experience to decipher the interplay between chromatin accessibility, 3D-chromatin architecture and transcriptional changes across different memory phases. Non activated (basal) and activated neurons during memory encoding (early), consolidation (late) and recall (reactivated) were sorted and subjected to nuclear RNA sequencing (nRNA-seq) to determine gene expression, ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) to assess chromatin accessibility, chromosome conformation capture (Hi-C) to identify global 3D -genome architecture and promoter capture Hi-C to identify the long range promoter-enhancer interactions. Results: Our analysis revealed dynamic changes in compartments organization, where we observed re-localization of large chromatin segments from inactive to permissive environment (and vice versa) during the initial and late phase of memory formation. Interestingly, 52% of the regions in the early phase that switched from B to A maintained that state in the late phase (i.e. remained in state A. Moreover, nearly all these regions significantly overlapped with gained DARs identified in our ATAC-seq analysis, confirming the transition of sub-compartment from inactive to permissive environment. This data indicates that while some loci undergo sub-compartment switching across different memory phases, the majority are stable, correlate with chromatin accessibility and therefore might contribute to long-term changes in neuronal properties and function after initial activation.

2020-06-23 | GSE152953 | GEO

Multi-scale epigenomic priming of inflammatory genes enables rapid recall in human memory T helper cells [ChIP-seq]

Project description:Memory T cells provide long-lasting defense responses through their ability to rapidly reactivate. How memory T cells efficiently ‘recall’ an inflammatory transcriptional program remains unclear. Here, we show that primary human CD4+ memory T helper (Th) cells carry three distinct activation-inducible recall gene modules that drive metabolic adaptation, T cell activation and inflammatory cytokine production. Enhancer elements controlling recall genes were epigenetically primed through the local maintenance of transcription-permissive chromatin in resting memory Th cells. At the three-dimensional level, recall genes clustered in transcriptionally permissive subnuclear compartments and resided in topologically associating domains (‘memory TADs’), in which activation-associated promoter-enhancer interactions were pre-formed. This primed epigenomic landscape was exploited by AP-1 transcription factors - including MAF - to promote rapid transcriptional activation. Finally, recall genes and their enhancers were linked to memory Th cell dysfunction in chronic inflammatory disease. Together, our results implicate multi-scale epigenomic priming - comprising a specialized three-dimensional chromatin organization - as a key mechanism underlying immunological memory.

2023-08-08 | GSE211023 | GEO

Multi-scale epigenomic priming of inflammatory genes enables rapid recall in human memory T helper cells [RNA-seq]

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Establishment, Maintenance and Recall of Inflammatory Memory

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Project description:Members of the BTB-ZF transcription factor family regulate the immune system. Our lab identified that family member Zbtb20 contributes to the differentiation, recall responses and metabolism of CD8 T cells. Here, we report a characterization of the transcriptional and epigenetic signatures controlled by Zbtb20 at single-cell resolution during the effector and memory phases of the CD8 T cell response. Without Zbtb20, transcriptional programs associated with memory CD8 T cell formation were upregulated throughout the CD8 T response. A signature of open chromatin was associated with genes controlling T cell activation, consistent with the known impact on differentiation. Additionally, memory CD8 T cells lacking Zbtb20 were characterized by open chromatin regions with overrepresentation of AP-1 transcription factor motifs and elevated RNA- and protein-level expression of the corresponding AP-1 components. Finally, we describe motifs and genomic annotations from the DNA targets of Zbtb20 in CD8 T cells identified by CUT&RUN. Together, these data establish the transcriptional and epigenetic networks contributing to the control of CD8 T cell responses by Zbtb20.

2023-07-03 | GSE234575 | GEO

Characterizing control of memory CD8 T cell differentiation by BTB-ZF transcription factor Zbtb20 using single cell RNA-sequencing (scATAC-Seq)

2023-07-03 | GSE234574 | GEO

Characterizing control of memory CD8 T cell differentiation by BTB-ZF transcription factor Zbtb20 using single cell RNA-sequencing (CUT&RUN)

2023-07-03 | GSE234573 | GEO

The histone chaperone Anp32e regulates memory formation, transcription and dendritic morphogenesis by regulating steady-state H2A.Z binding in neurons

Project description:Rapid removal of the histone variant H2A.Z from neural chromatin is a key step in learning-induced gene expression and memory formation, but the molecular mechanisms underlying learning-induced H2A.Z removal are unknown. Anp32e was recently identified an H2A.Z-specific histone chaperone that removes H2A.Z from nucleosomes in dividing cells, but whether it plays a similar role in non-dividing neurons is unknown. Moreover, prior studies only investigated effects of Anp32e on H2A.Z binding under steady state-conditions, such that its effect on H2A.Z removal under stimulus-induced conditions is unknown. Here, we show that Anp32e regulates H2A.Z binding in neurons under steady-state conditions, but that stimulus-induced H2A.Z removal is largely independent of Anp32e. In assessing the functional consequences of Anp32e, we showed that its depletion leads to H2A.Z-dependent impairment in dendritic arborization in cultured hippocampal neurons, as well as impaired recall of contextual fear memory and transcriptional regulation. Together, these data indicate the Anp32E regulates behavioral and morphological outcomes by preventing H2A.Z accumulation in chromatin rather than by regulating activity-mediated H2A.Z dynamics.

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