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Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator

ABSTRACT: Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator

PROVIDER: PRJNA400914 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5996660.fastq.gz	Fastqsanger.gz
	SRR5996670.fastq.gz	Fastqsanger.gz
	SRR5996651.fastq.gz	Fastqsanger.gz
	SRR5996661.fastq.gz	Fastqsanger.gz
	SRR5996671.fastq.gz	Fastqsanger.gz

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Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator [RNA-Seq]

Project description:In the adult brain, histone acetylation is associated with activity-regulated transcriptional changes that are required for synaptic plasticity and memory. These processes are dismantled in neurodegenerative diseases. Here, we demonstrate that synaptic plasticity and memory deficiencies can be restored in a mouse model of tauopathy following treatment with CSP-TTK21, a small molecule activator of CBP/p300 histone acetyltransferases (HAT). CSP-TTK21 normalized the H2B acetylation levels in many genes, including a series of super-enhancer –regulated genes, associated with plasticity and neuronal function in resting tauopathic mice. CSP-TTK21 re-established part of the learning-induced hippocampal transcriptome, including the induction of immediate early genes and memory-related genes, and the down-regulation of neuronal identity genes that bear super-enhancers. This study is the first to provide in vivo proof-of-concept evidence that direct activation of CBP/p300 HAT efficiently and selectively reverses epigenetic, transcriptional, synaptic plasticity, and behavioral deficits associated to Alzheimer’s disease lesions in mice.

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Epigenetic correction of defective plasticity in a tauopathy mouse model with an acetyltransferase activator

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Project description:Chromatin acetylation, a critical regulator of synaptic plasticity and memory processes, is thought to be altered in neurodegenerative diseases. Here, we demonstrate that spatial memory and plasticity (LTD, dendritic spine formation) deficits can be restored in a mouse model of tauopathy following treatment with CSP-TTK21, a small-molecule activator of CBP/p300 histone acetyltransferases (HAT). At the transcriptional level, CSP-TTK21 re-established half of the hippocampal transcriptome in learning mice, likely through increased expression of neuronal activity genes and memory enhancers. At the epigenomic level, the hippocampus of tauopathic mice showed a significant decrease in H2B but not H3K27 acetylation levels, both marks co-localizing at TSS and CBP enhancers. Importantly, CSP-TTK21 treatment increased H2B acetylation levels at decreased peaks, CBP enhancers, and TSS, including genes associated with plasticity and neuronal functions, overall providing a 95% rescue of the H2B acetylome in tauopathic mice. This study is the first to provide in vivo proof-of-concept evidence that CBP/p300 HAT activation efficiently reverses epigenetic, transcriptional, synaptic plasticity, and behavioral deficits associated with Alzheimer's disease lesions in mice.

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Reinstating plasticity and memory in a tauopathy mouse model with an acetyltransferase activator

Project description:Chromatin acetylation, a critical regulator of synaptic plasticity and memory processes, is thought to be altered in neurodegenerative diseases. Here, we demonstrate that spatial memory and plasticity (LTD, dendritic spine formation) deficits can be restored in a mouse model of tauopathy following treatment with CSP-TTK21, a small molecule activator of CBP/p300 histone acetyltransferases (HAT). At the transcriptional level, CSP-TTK21 re-established half of the hippocampal transcriptome in learning mice, likely through increased expression of neuronal activity genes and memory enhancers. At the epigenomic level, the hippocampus of tauopathic mice showed a significant decrease of H2B but not H3K27 acetylation levels, both marks co-localizing at TSS and CBP enhancers. Importantly, CSP-TTK21 treatment increased H2B acetylation levels at decreased peaks, CBP enhancers and TSS, including genes associated with plasticity and neuronal functions, overall providing a 95% rescue of the H2B acetylome in tauopathic mice. This study is the first to provide in vivo proof-of-concept evidence that CBP/p300 HAT activation efficiently reverses epigenetic, transcriptional, synaptic plasticity, and behavioral deficits associated with Alzheimer's disease lesions in mice.

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