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Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models [ChIP-seq]

ABSTRACT: Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models [ChIP-seq]

PROVIDER: PRJNA796040 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17540864.fastq.gz	Fastqsanger.gz
	SRR17540865.fastq.gz	Fastqsanger.gz
	SRR17540866.fastq.gz	Fastqsanger.gz
	SRR17540867.fastq.gz	Fastqsanger.gz
	SRR17540868.fastq.gz	Fastqsanger.gz

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Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models

Project description:Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models

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Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models [RNA-seq]

Project description:Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models [RNA-seq]

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Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models [RNA-seq]

Project description:We performed RNAseq experiments to examine genome-wide transcriptional changes in PFC of Shank3 +/∆C mice with or without GSK-LSD1 treatment.

2022-01-13 | GSE193380 | GEO

Targeting histone demethylase LSD1 for treatment of deficits in autism mouse models.

Project description:Large-scale genetic studies have revealed that the most prominent genes disrupted in autism are chromatin regulators mediating histone methylation/demethylation, suggesting the central role of epigenetic dysfunction in this disorder. Here, we show that histone lysine 4 dimethylation (H3K4me2), a histone mark linked to gene activation, is significantly decreased in the prefrontal cortex (PFC) of autistic human patients and mutant mice with the deficiency of top-ranking autism risk factor Shank3 or Cul3. A brief treatment of the autism models with highly potent and selective inhibitors of the H3K4me2 demethylase LSD1 (KDM1A) leads to the robust rescue of core symptoms of autism, including social deficits and repetitive behaviors. Concomitantly, LSD1 inhibition restores NMDA receptor function in PFC and AMPA receptor-mediated currents in striatum of Shank3-deficient mice. Genome-wide RNAseq and ChIPseq reveal that treatment of Shank3-deficient mice with the LSD1 inhibitor restores the expression and H3K4me2 occupancy of downregulated genes enriched in synaptic signaling and developmental processes. The immediate early gene tightly linked to neuronal plasticity, Egr1, is on the top list of rescued genes. The diminished transcription of Egr1 is recapitulated in PFC of autistic human patients. Overexpression of Egr1 in PFC of Shank3-deficient mice ameliorates social preference deficits. These results have for the first time revealed an important role of H3K4me2 abnormality in ASD pathophysiology, and the therapeutic potential of targeting H3K4me2 demethylase LSD1 or the downstream molecule Egr1 for ASD.

| S-EPMC9477974 | biostudies-literature

Epigenetic Rescue of Autism-like Social Deficits in Shank3-Deficient Mouse Models

Project description:Epigenetic Rescue of Autism-like Social Deficits in Shank3-Deficient Mouse Models

| PRJNA430439 | ENA

Uncoupling Histone Modification Crosstalk by Engineering Lysine Demethylase LSD1

Project description:Biochemical crosstalk between two or more histone modifications is often observed in epigenetic enzyme regulation but its functional significance in cells has been difficult to discern. Prior enzymatic studies have revealed that Lys14 acetylation of histone H3 can inhibit Lys4 demethylation by lysine specific demethylase 1 (LSD1). Here we have engineered a mutant form of LSD1, Y391K, which renders the nucleosome demethylase activity of LSD1 insensitive to Lys14 acetylation. Y391K LSD1 knockin cells show increased repression of a set of genes associated with cellular adhesion. Chromatin profiling revealed that the cis-regulatory regions of these silenced genes display a higher level of H3 Lys14 acetylation than the baseline in unedited, parental cells. Y391K LSD1 knockin cells show diminished H3 mono-methyl Lys4 in the vicinity of these silenced genes, consistent with a role for enhanced LSD1 demethylase activity in these regions. These findings illuminate the functional consequences of disconnecting histone modification crosstalk for a key epigenetic enzyme in gene and chromatin regulation.

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Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models

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

2022-01-13 | GSE193405 | GEO

Uncoupling Histone Modification Crosstalk by Engineering Lysine Demethylase LSD1 [RNA-seq]

2024-05-08 | GSE243427 | GEO

Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia

Project description:This SuperSeries is composed of the following subset Series: GSE34672: Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia [Illumina HumanHT-12 gene expression array] GSE34725: Inhibition of the LSD1 (KDM1A) demethylase reactivates the all-trans-retinoic acid differentiation pathway in acute myeloid leukemia [ChIP-Seq] Refer to individual Series

2012-03-14 | E-GEOD-34726 | biostudies-arrayexpress

LSD1 inhibtion in NEPC cell line models.

Project description:Lysine-specific demethylase 1 (LSD1) is a histone demethylase that promotes stemness and cancer cell survival, including in prostate cancer. Most prostate malignancies are adenocarcinomas with luminal differentiation. However, a subset of tumors undergoes cellular reprogramming to a more lethal neuroendocrine prostate cancer (NEPC) with neuronal differentiation. The frequency of NEPC is increasing since widespread use of potent androgen receptor signaling inhibitors. Currently, there are no effective treatments for NEPC. We previously determined that LSD1 promotes survival of prostate adenocarcinoma tumors. However, role of LSD1 in NEPC is largely unknown. We sought to identify key genes and molecular pathways controlled by LSD1 in NEPC. We therefore inhibited LSD1 with SP2509 and performed RNA-seq in LASCPC-01, LNCaP-N-Myc, and MR42D cell lines. The vast majority of differentially expressed genes after SP2509 treatment were upregulated, suggesting that LSD1 may primarily function as a transcriptional repressor in NEPC. RNA-seq analysis reveals that LSD1 represses pathways linked to luminal differentiation and TP53 is the top pathway reactivated after LSD1 suppression. Taken together, these data suggest that LSD1 may be an important regulator of TP53 function in prostate cancer.

2023-08-30 | GSE218993 | GEO

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