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Single-cell 5-hydroxymethyl cytosine dynamics during remote memory formation

ABSTRACT: Single-cell 5-hydroxymethyl cytosine dynamics during remote memory formation

PROVIDER: PRJNA1070287 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27754200_1.fastq.gz	Fastqsanger.gz
	SRR27754200_2.fastq.gz	Fastqsanger.gz
	SRR27754201_1.fastq.gz	Fastqsanger.gz
	SRR27754201_2.fastq.gz	Fastqsanger.gz
	SRR27754202_1.fastq.gz	Fastqsanger.gz

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Single-cell 5-hydroxymethyl cytosine dynamics during remote memory formation

Project description:We introduce the Split-Pool based Epigenetic Decoding (SPEED) method, a combinatorial barcoding strategy enhancing the throughput of single-cell 5-hydroxymethyl cytosine (5hmC) or 5-methylcytosine (5mC) profiling. SPEED enables simultaneous, unbiased examination of 5hmC traits across distinct brain regions, surpassing limitations of individual cell scrutiny. Using SPEED we unveil dynamic 5hmC patterns linked to remote memory formation in the brain.

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Epigenetic priming of memory updating during reconsolidation to attenuate remote fear memories

Project description:Remembrances of traumata range among the most enduring forms of memories. Despite the elevated lifetime prevalence of anxiety disorders, effective strategies to attenuate long-term traumatic memories are scarce. The most efficacious treatments to diminish recent (i.e., day-old) traumata capitalize on memory updating mechanisms during reconsolidation that are initiated upon memory recall. Here, we show that in mice successful reconsolidation-updating paradigms for recent memories fail to attenuate remote (i.e., month-old) ones. We find that whereas recent memory recall induces a limited period of hippocampal neuroplasticity mediated, in part, by S-nitrosylation of HDAC2 and histone acetylation, such plasticity is absent for remote memories. However, by using an HDAC2-targeting inhibitor (HDACi) during reconsolidation, even remote memories can be persistently attenuated. This intervention epigenetically primes the expression of neuroplasticity-related genes as revealed by whole genome RNA sequencing, which is accompanied by higher metabolic, synaptic and structural plasticity. Thus, applying HDACis during memory reconsolidation might constitute a treatment option for remote traumata. 3 biological replicates per group were analyzed. The material analyzed was whole hippocampi from one brain hemisphere, from which total RNA was extracted.

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High-throughput exploration of single-cell transcriptional alterations associated with remote fear memory formation

Project description:Leveraging SPEED in tandem with snRNA-Seq, we uncover molecular identities of distinct neural subtypes, concurrent 5hmC alterations at active enhancers and gene bodies, and dynamic gene expression associated with remote memory formation. This comprehensive analysis encompasses several thousand cells from the cerebral and cerebellar cortex of home-caged (HC) and fear-conditioned (FC) mice.

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Epigenetic priming of memory updating during reconsolidation to attenuate remote fear memories

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Persistent transcriptional programs are associated with remote memory in diverse cells of the medial prefrontal cortex

Project description:single cell RNAseq of remote memory engram cells from the murine mPFC

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Remote memory and cortical synaptic plasticity require neuronal CCCTC-binding factor (CTCF), a central organizer of 3D chromatin architecture

Project description:Molecular mechanism of long-term memory has been extensively studied in the context of hippocampus-dependent recent memory examined within several days; however, months-old remote memory maintained in the cortex for long-term has not much been investigated at molecular levels yet. Various epigenetic mechanisms are known to be important for long-term memory, but how 3D chromatin architecture and its regulator molecules contribute to neuronal plasticity and memory consolidation are still largely unknown. To assess memory upon perturbation of 3D chromatin structure, we chose CCCTC-binding factor (CTCF), a seven-zinc finger protein well known for its role as a transcription factor and a chromatin regulator, and created the conditional knockout (cKO) mice, in which CTCF is lost in neurons during adulthood. Our CTCF cKO mice showed normal recent memory in contextual fear conditioning and spatial water maze task. However, they showed remarkable impairments in remote memory in both tasks. Underlying the remote memory-specific phenotypes, we found that loss of CTCF disrupts cortical long-term potentiation (LTP) but not hippocampal LTP. Through RNA-sequencing, we found that CTCF KD cultured cortical neurons have altered the expression of hundreds of genes, some of which we uncovered to be regulated by neuronal activity. These results suggest that remote memory storage in the cortex requires CTCF-mediated chromatin regulation in neurons while recent memory formation in the hippocampus does not.

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Tet-dependent 5-hydroxymethyl-Cytosine modification of mRNA regulates axon guidance genes in Drosophila

Project description:Tet-dependent 5-hydroxymethyl-Cytosine modification of mRNA regulates axon guidance genes in Drosophila

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Strain differences in responsiveness to chronic restraint stress affect remote contextual fear memory and blood transcriptomics

Project description:Fear memory regulation is thought to be similar between humans and animals, and the role of stress in altering remote memory is little explored. Since individual variation in stress reactivity exists, should stress alter remote memory, invividuals with differing stress-reactivity would affect it to various degree. We evaluate this question using two strains of rats with differing stress-reactivity. The Fisher 344 (F344) strain is known to have active coping style and represent normal stress-reactivity, while the Wistar–Kyoto (WKY) rat shows passive coping strategies and heightened stress-reactivity. Male animals were exposed contextual fear conditioning (CFC) and four weeks later, chronic restraint stress (CRS) or no stress (NS) was administered for two weeks. Remote memory, immediate stress response to a second CFC, and reinstated fear memory was measured. Both recent and reinstated fear memory were greater in F344s, regardless of the stress status, In contrast, remote memory was attenuated in F344 only, concurring with their increased immediate stress responsive behavior after CRS. To find if this strain-specific response to CRS can be mirrored by transcriptomic changes in the blood, RNA sequencing was carried out. Overlapping differentially expressed genes (DEGs) between NS vs. CRS in the blood of F344 and WKY suggest a convergence of stress-related molecular mechanisms, independent of stress-reactivity. In contrast, DEGs unique to the F344 and the WKY stress responses are divergent in their functionality and networks, beyond that of strain differences in their non-stressed state. These unique DEGs than could be implicated as biomarkers stress-reactivity.

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High-throughput exploration of single-cell transcriptional alterations associated with remote fear memory formation

Project description:High-throughput exploration of single-cell transcriptional alterations associated with remote fear memory formation

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Specific loss of remote fear memory by knockdown of a neuron-specific nucleosome remodeling factor BAF53b in the amygdala

Project description:Despite recent advances, molecular events and mechanisms involved in long-lasting memory formation are unclear. Here, we report a critical role for nucleosome remodeling factor BAF53b in mice. We observed an increase of BAF53b expression beyond 24 h after fear conditioning in the lateral amygdala, which was crucial for memory retention at remote time. RNA-seq analyses and behavioral rescue experiments identified fibroblast growth factor-1 (FGF1) as a candidate downstream effector.

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