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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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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.

2018-11-05 | GSE103359 | GEO

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

2018-11-05 | GSE103358 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-11-05 | GSE103360 | GEO

Mus musculus

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

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Mus musculus

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Increase genome editing efficiency by Cas9 transcriptional activator and histone acetyltransferase activator

Project description:Increase genome editing efficiency by Cas9 transcriptional activator and histone acetyltransferase activator

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Increase genome editing efficiency by Cas9 transcriptional activator and histone acetyltransferase activator

Project description:The CRISPR/Cas9 system shows diverse levels of genome editing activities on eukaryotic genomic DNA targets, and experiments desire high-efficiency targets. Here we show that chromatin open status is a pivotal determinant of the Cas9 editing activity in mammalian cells, and increasing chromatin accessibility can efficiently improve Cas9 genome editing activity. However, the strategy that fusing the VP64 transcriptional activation domain at the C-terminus of Cas9 can only promote genome editing activity slightly at most tested CRISPR/Cas9 targets in Lenti-X 293T cells. Because histone acetylation increases eukaryotic chromatin accessibility, we further improve genome editing by elevating histone acetylation. We demonstrate that promoting histone acetylation using histone acetyltransferase (HAT) activator YF-2 can improve genome editing from Cas9 and more robustly from the Cas9 transcriptional activator. This provides a strategy to improve CRISPR/Cas9 genome editing activity and enables broader gRNA target choices in eukaryotes.

2022-04-21 | GSE200943 | GEO

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

Project description: Not available

| S-EPMC6220301 | biostudies-literature

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

Project description: Not available

| S-SCDT-EMM-2017-08587-T | biostudies-other

Gene expression profile of Tra1 GID (Gal4 interaction defective) mutants

Project description:Promoter-specific transcriptional activators (activators) stimulate transcription through direct interactions with one or more components of the transcription machinery, termed the “target”. Previous studies have provided evidence that the Tra1 subunit of the yeast SAGA (Spt-Ada-Gcn5-acetyltransferase) complex is the target of the yeast activator Gal4. However, several other general transcription factors, in particular the mediator complex, have also been implicated as Gal4 targets. To investigate the essentiality of Tra1 as a target of Gal4, here we derive Tra1 mutants that are selectively defective for interaction with Gal4 in vivo (Gal4 Interaction Defective (GID) mutants). In contrast to wild-type Tra1, Tra1 GID mutants are not recruited by Gal4 to the promoter and cannot support Gal4-directed transcription activation, demonstrating that the Gal4–Tra1 interaction is required for Gal4 function. In yeast strains expressing a Tra1 GID mutant, Gal4 promoter binding is unexpectedly also diminished indicating that Gal4 and Tra1 bind cooperatively. Consistent with cooperative binding, we demonstrate that the interaction between Gal4 and Tra1 occurs predominantly on the promoter and not off DNA. Finally, we show that although Tra1 is also targeted by other activators, these interaction are unaffected by GID mutations, revealing an unanticipated specificity of the Gal4-Tra1 interaction. 3 samples were analyzed in duplicate with completely randomized design

2011-12-30 | E-GEOD-31389 | biostudies-arrayexpress

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