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TAK-418-418, a LSD1 inhibitor, can rescue the genome wide chromatin abnormality in hippocapmus tissue in KMT2D+/bGeo mice after 2 week treatment [ChIP-seq]

ABSTRACT: KMT2D+/bGeoation in KMT2D, a histone-lysine N-methyl transferase, is responsible for majority of Kabuki syndrome in human. A mouse model of Kabuki syndrome with heterzygous KMT2D+/bGeoation of KMT2D, KMT2D+/bGeo was created to understand the disease mechanism and for drug discovery. TAK-418-418, a lysine-specific histone demethylase (LSD1) inhibitor, was tested on these mice for therapeutic treatment of the disease. Rescue of genome wide chromatin abnormality, which has been reported in KMT2D+/bGeo mice, was evaluated by high throughput next generation sequencing following chromatin immunoprecipitation of H3K4me1 and H3K4me3.

ORGANISM(S): Mus musculus

PROVIDER: GSE146727 | GEO | 2020/03/11

REPOSITORIES: GEO

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TAK-418-418, a LSD1 inhibitor, can rescue the genome wide chromatin abnormality in hippocapmus tissue in KMT2D+/bGeo mice after 2 week treatment [RNA-seq]

Project description:Mutation in KMT2D, a histone-lysine N-methyl transferase, is responsible for majority of Kabuki syndrome in human. A mouse model of Kabuki syndrome with heterzygous mutation of KMT2D, KMT2D+/bGeo was created to understand the disease mechanism and for drug discovery. TAK-418-418, a lysine-specific histone demethylase (LSD1) inhibitor, was tested on these mice for therapeutic treatment of the disease. Differences between expression levels among different experimental conditions was evaluated by high throughput RNA sequencing (RNA-Seq).

2020-03-11 | GSE146728 | GEO

DNA methylation profile in animal models of neurodevelopmental disorders treated with TAK-418

Project description:We report the DNA methylation profiles in the brain cortex of animal models of neurodevelopmental disorders (rat with prenatal exposure to valproate and mouse with prenatal exposure to poly I:C) treated with TAK-418.

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RNA expression profile in animal models of neurodevelopmental disorders treated with TAK-418

Project description:We report the RNA expression profiles in the brain cortex of animal models of neurodevelopmental disorders (rat with prenatal exposure to valproate and mouse with prenatal exposure to poly I:C) treated with TAK-418.

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Histone modification profile in animal models of neurodevelopmental disorders treated with TAK-418

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TAK-418-418, a LSD1 inhibitor, can rescue the genome wide chromatin abnormality in hippocapmus tissue in KMT2D+/bGeo mice after 2 week treatment

Project description:TAK-418-418, a LSD1 inhibitor, can rescue the genome wide chromatin abnormality in hippocapmus tissue in KMT2D+/bGeo mice after 2 week treatment

| PRJNA611772 | ENA

Animal models of neurodevelopmental disorders treated with TAK-418

Project description:Animal models of neurodevelopmental disorders treated with TAK-418

| PRJNA695298 | ENA

TAK-418-418, a LSD1 inhibitor, can rescue the genome wide chromatin abnormality in hippocapmus tissue in KMT2D+/bGeo mice after 2 week treatment [ChIP-seq]

Project description:TAK-418-418, a LSD1 inhibitor, can rescue the genome wide chromatin abnormality in hippocapmus tissue in KMT2D+/bGeo mice after 2 week treatment [ChIP-seq]

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TAK-418-418, a LSD1 inhibitor, can rescue the genome wide chromatin abnormality in hippocapmus tissue in KMT2D+/bGeo mice after 2 week treatment [RNA-seq]

Project description:TAK-418-418, a LSD1 inhibitor, can rescue the genome wide chromatin abnormality in hippocapmus tissue in KMT2D+/bGeo mice after 2 week treatment [RNA-seq]

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A ketogenic diet rescues hippocampal memory defects in a mouse model of Kabuki syndrome

Project description:Kabuki syndrome is a Mendelian intellectual disability syndrome caused by mutations in either of two genes (KMT2D and KDM6A) involved in chromatin accessibility. We previously showed that an agent that promotes chromatin opening, the histone deacetylase inhibitor (HDACi) AR-42, ameliorates the deficiency of adult neurogenesis in the granule cell layer of the dentate gyrus, and rescues hippocampal memory defects in a mouse model of Kabuki syndrome (Kmt2d+/βGeo). Unlike a drug, a dietary intervention could be quickly transitioned to the clinic. Therefore, we have explored whether treatment with a ketogenic diet could lead to a similar rescue through increased amounts of beta-hydroxybutyrate, an endogenous HDACi. Here, we report that a ketogenic diet in Kmt2d+/βGeo mice modulates H3ac and H3K4me3 in the granular cell layer, with concomitant rescue of both the neurogenesis defect and hippocampal memory abnormalities seen in Kmt2d+/βGeo mice; similar effects on neurogenesis were observed upon exogenous administration of beta-hydroxybutyrate. These data suggests that dietary modulation of epigenetic modifications through elevation of beta-hydroxybutyrate may provide a feasible strategy to treat the intellectual disability seen in Kabuki syndrome and related disorders. We used microarrays to query global gene expression changes in the hippocampus of wild type and Kmt2d+/βGeo (Kabuki syndrome model) mice on a regular diet to identify specific gene expression abnormalities in the hippocampus of the Kabuki syndrome mouse model.

2016-12-03 | GSE90836 | GEO

Patients with a Kabuki syndrome phenotype demonstrate DNA methylation abnormalities.

Project description:Kabuki syndrome is a monogenic disorder caused by loss of function variants in either of two genes encoding histone-modifying enzymes. We performed targeted sequencing in a cohort of 27 probands with a clinical diagnosis of Kabuki syndrome. Of these, 12 had causative variants in the two known Kabuki syndrome genes. In 2, we identified presumptive loss of function de novo variants in KMT2A (missense and splice site variants), a gene that encodes another histone modifying enzyme previously exclusively associated with Wiedermann-Steiner syndrome. Although Kabuki syndrome is a disorder of histone modification, we also find alterations in DNA methylation among individuals with a Kabuki syndrome diagnosis relative to matched normal controls, regardless of whether they carry a variant in KMT2A or KMT2D or not. Furthermore, we observed characteristic global abnormalities of DNA methylation that distinguished patients with a loss of function variant in KMT2D or missense or splice site variants in either KMT2D or KMT2A from normal controls. Our results provide new insights into the relationship of genotype to epigenotype and phenotype and indicate cross-talk between histone and DNA methylation machineries exposed by inborn errors of the epigenetic apparatus.

2018-06-27 | GSE116300 | GEO

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