Protein phosphatase 1-dependent transcriptional programs for long-term memory and plasticity

Gräff, Johannes; Koshibu, Kyoko; Jouvenceau, Anne; Dutar, P.; Mansuy, Isabelle M.

doi:10.1101/lm.1766510

Cited by 54 publications

(36 citation statements)

References 66 publications

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“…Adult (3-6 months old) male double transgenic mice carrying a fragment including amino acids 143 to 224 of the nuclear inhibitor of PP1 (NIPP1*) linked to a bidirectional tetO (BiTetO) promoter with a LacZ reporter gene (Transgenic) were used as described 22 . To obtain double transgenic animals, these mice were crossed with mice expressing a reverse tetracycline-controlled transactivator (rtTA2) under the control of the forebrain-specific CaMKIIα promoter 40 .…”

Section: Methodsmentioning

confidence: 99%

“…To further examine the relevance of histones marks for memory consolidation, we took advantage of a recently developed transgenic mouse model 22 , in which memory is enhanced by inhibition of the chromatin regulator and memory suppressor PP1 23 . In this model, PP1 is selectively inhibited in forebrain neurons, in particular in the hippocampus and PFC ( Supplementary Fig.…”

Section: Hippocampal Histone Ptms Are Induced Rapidly But Transientlymentioning

confidence: 99%

“…In this model, PP1 is selectively inhibited in forebrain neurons, in particular in the hippocampus and PFC ( Supplementary Fig. S3) 13,14,22 . When tested on the object recognition task, the transgenic mice (Transgenic) had memory performance comparable to control mice (Control) 10 min after training but had improved memory both 1 and 7 days after training (Fig.…”

Section: Hippocampal Histone Ptms Are Induced Rapidly But Transientlymentioning

confidence: 99%

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Dynamic histone marks in the hippocampus and cortex facilitate memory consolidation

et al. 2012

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memory consolidation requires a timely controlled interplay between the hippocampus, a brain region important for memory formation, and the cortex, a region recruited for memory storage. Here we show that memory consolidation is associated with specific epigenetic modifications on histone proteins that have a distinct dynamic in these brain areas. While in the hippocampus, histone post-translational modifications (PTms) are rapidly and transiently activated after learning, in the cortex they are induced with delay but persist over time. When these histone PTms are increased in vivo by transgenic intervention or intense training, they facilitate memory consolidation. Conversely, when they are pharmacologically blocked, memory consolidation is impaired. These histone PTms are further associated with the expression of the immediate early gene zif268, a transcription factor that favours memory consolidation. These findings reveal the spatiotemporal dynamics of histone marks during memory consolidation, and demonstrate their inherent 'mnemonic' property.

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Section: Methodsmentioning

confidence: 99%

Section: Hippocampal Histone Ptms Are Induced Rapidly But Transientlymentioning

confidence: 99%

Section: Hippocampal Histone Ptms Are Induced Rapidly But Transientlymentioning

confidence: 99%

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Dynamic histone marks in the hippocampus and cortex facilitate memory consolidation

et al. 2012

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“…MSK is a histone kinase that is activated by ERK signaling ( Figure 1). Interestingly, decreasing histone phosphorylation through mutations in MSK causes defects in the spatial memory in mice, while enhancing histone phosphorylation by deletion of the histone phosphatase PP1 can improve spatial memory (63)(64)(65). Thus, in parallel with histone acetylation, increased histone phosphorylation appears to enhance memory formation.…”

Section: Histone Phosphorylationmentioning

confidence: 99%

“…However, these studies do not reveal the true mechanism or extent of gene regulation in learning and memory. Some studies have used a genome wide approach to determine how epigenetic regulators influence gene expression in the brain (30,57,64,77,78). Genome wide mRNA profiling has been performed in animals that have mutations in epigenetic regulators that are known to cause learning and memory defects.…”

Section: Targets Of Epigenetic Control In Learning and Memorymentioning

confidence: 99%

Epigenetic regulation of memory: implications in human cognitive disorders

Kramer

2013

BioMolecular Concepts

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Epigenetic modification of chromatin structure is an important mechanism in the regulation of gene expression. Recent studies have shown that dynamic regulation of chromatin structure occurs in response to neuronal stimulation associated with learning and memory. Learning-induced chromatin modifications include DNA methylation, histone acetylation, histone phosphorylation and histone methylation. Studies in animal models have used genetic and pharmacological methods to manipulate the epigenetic machinery in the brain during learning and memory formation. In general, these studies suggest that epigenetic regulation of chromatin structure is essential for long term memory (LTM) consolidation, which is known to require new gene transcription. Analysis of animal models has also implicated epigenetic mechanisms in impaired cognition associated with aging, neurodegenerative disease, and intellectual disability (ID). Recently, it has been shown that a subset of ID disorders and autism are caused by disruption of specific chromatin modification complexes that are involved in nuclear hormone receptor mediated transcriptional regulation. This review provides an overview of chromatin modifications that are implicated in learning and memory and discusses the role of chromatin modifying proteins in learning-induced transcriptional regulation and human cognitive disorders.

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Serine/threonine‐protein phosphatase 1 α levels are paralleling olfactory memory formation in the CD1 mouse

et al. 2011

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Although olfactory discrimination has already been studied in several mouse strains, data on protein levels linked to olfactory memory are limited. Wild mouse strains Mus musculus musculus, Mus musculus domesticus and CD1 laboratory outbred mice were tested in a conditioned odor preference task and trained to discriminate between two odors, Rose and Lemon, by pairing one odor with a sugar reward. Six hours following the final test, mice were sacrificed and olfactory bulbs (OB) were taken for gel-based proteomics analyses and immunoblotting. OB proteins were extracted, separated by 2-DE and quantified using specific software (Proteomweaver). Odor-trained mice showed a preference for the previously rewarded odor suggesting that conditioned odor preference occurred. In CD1 mice levels, one out of 482 protein spots was significantly increased in odor-trained mice as compared with the control group; it was in-gel digested by trypsin and chymotrypsin and analyzed by tandem mass spectrometry (nano-ESI-LC-MS/MS). The spot was unambiguously identified as serine/threonine-protein phosphatase PP1-α catalytic subunit (PP-1A) and differential levels observed in gel-based proteomic studies were verified by immunoblotting. PP-1A is a key signalling element in synaptic plasticity and memory processes and is herein shown to be paralleling olfactory discrimination representing olfactory memory.

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Protein phosphatase 1-dependent transcriptional programs for long-term memory and plasticity

Cited by 54 publications

References 66 publications

Dynamic histone marks in the hippocampus and cortex facilitate memory consolidation

Dynamic histone marks in the hippocampus and cortex facilitate memory consolidation

Epigenetic regulation of memory: implications in human cognitive disorders

Serine/threonine‐protein phosphatase 1 α levels are paralleling olfactory memory formation in the CD1 mouse

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