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MiRNA-seq and RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE189250 | GEO | 2021/11/24

REPOSITORIES: GEO

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RNA-seq and miRNA-seq data from pharmacological inhibition of the G9a/GLP histone methyltransferase complex with UNC0642 in SAMP8 mice.

Project description:Growing evidence demonstrates the epigenetic modulation as a key event in Alzheimer's disease (AD) pathology. Furthermore, recent data suggests that the epigenetic regulation by the methyltransferase G9a is a crucial mechanism involved in learning and memory formation. Taking this into account, we hereby provide genomics data from pharmacological intervention with UNC0642, a potent and selective G9a/GLP in SAMP8 mice, a model of Alzheimer's disease (AD). We have generated novel RNA-seq and miRNA-seq data for three groups, healthy SAMR1, SAMP8 control and SAMP8 treated with UNC0642 (5 mg/Kg). Thus, the new data can be used to find miRNA regulation, and the mRNA's modified in AD under G9a/GLP inhibition.

| S-EPMC8257974 | biostudies-literature

miRNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

Project description:Purpose: The aim of this study is to compare brain transcriptome profile (RNA-seq) after G9a inhibition. Methods: Hippocampus profiles of 7-month-old SAMP8 Control and SAMP8 Treated mice groups were generated by deep sequencing, pooled using Ilumnia Hiseq. Results: G9a inhibition with UNC0642 induces a transcriptional profile that allows beneficial effects on cognitive performance. Differential expression analysis identified 697 differentially expressed genes (DEG) (fold change cutoff of ≥1.3, p-value<0.05). Of which 217 are reduced, and 480 are increased in SAMP8 UNC0642. Conclusions: Our study showed the first transcriptome analysis of whole brain after G9a inhibition, generated by RNA-seq technology, demonstrating transcriptomic changes.

2021-11-24 | GSE189248 | GEO

RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

2021-11-24 | GSE189249 | GEO

miRNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

Project description:miRNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

| PRJNA782199 | ENA

miRNA-seq and RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

Project description:miRNA-seq and RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

| PRJNA782198 | ENA

RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

Project description:RNA-seq data from pharmacological inhibition of the G9a histone methyltransferase with UNC0642 in SAMP8 mice

| PRJNA782200 | ENA

Inhibition of the G9a/GLP histone methyltransferase complex modulates anxiety-related behavior in mice.

Project description:Epigenetic gene-regulation abnormalities have been implicated in various neuropsychiatric disorders including schizophrenia and depression, as well as in the regulation of mood and anxiety. In addition, epigenetic mechanisms are involved in the actions of psychiatric drugs. Current anxiolytic drugs have significant shortcomings, and development of new medications is warranted. Two proteins, G9a (also known as EHMT2 or KMT1C) and GLP (G9a-like protein, also known as EHMT1 or KMT1D), which methylate lysine 9 of histone H3 (H3K9), could be promising anxiolytic targets. Postnatal genetic knock-out of G9a reduces anxiety-related behavior, consistent with the reduction of G9a levels by some medications used to treat anxiety (amitriptyline, imipramine and paroxetine). Conversely, there is increased anxiety-like behavior in mice with GLP haplodeficiency. We sought to determine whether two pharmacological inhibitors of G9a/GLP, UNC0642 and A-366, would have similar effects to genetic G9a/GLP insufficiency. We found that G9a/GLP inhibition with either compound reduced anxiety-like behaviors when administered to adult mice, in conjunction with decreased H3K9 methylation in the brain. In contrast, exposure to these compounds from embryonic day 9.5 (E9.5) until birth increased anxiety-like behaviors and decreased social interaction in adulthood, while H3K9 methylation was at normal levels in the brains of the adult mice. These findings reinforce genetic evidence that G9a/GLP has different effects on anxiety-like behavior at different stages of brain development, and suggest that targeting this histone methyltransferase pathway could be useful for developing new anxiolytic drugs. These data also suggest that antidepressant exposure in utero could have negative effects in adulthood, and further investigation of these effects is warranted.

| S-EPMC5943902 | biostudies-literature

Histone-lysine N-methyltransferase EHMT2 (G9a) inhibition mitigates tumorigenicity in Myc-driven liver cancer.

Project description:Hepatocellular carcinoma (HCC) is the third deadliest and sixth most common cancer in the world. Histone-lysine N-methyltransferase EHMT2 (also known as G9a) is a histone methyltransferase frequently overexpressed in many cancer types, including HCC. We showed that Myc-driven liver tumours have a unique H3K9 methylation pattern with corresponding G9a overexpression. This phenomenon of increased G9a was further observed in our c-Myc-positive HCC patient-derived xenografts. More importantly, we showed that HCC patients with higher c-Myc and G9a expression levels portend a poorer survival with lower median survival months. We demonstrated that c-Myc interacts with G9a in HCC and cooperates to regulate c-Myc-dependent gene repression. In addition, G9a stabilises c-Myc to promote cancer development, contributing to the growth and invasive capacity in HCC. Furthermore, combination therapy between G9a and synthetic-lethal target of c-Myc, CDK9, demonstrates strong efficacy in patient-derived avatars of Myc-driven HCC. Our work suggests that targeting G9a could prove to be a potential therapeutic avenue for Myc-driven liver cancer. This will increase our understanding of the underlying epigenetic mechanisms of aggressive tumour initiation and lead to improved therapeutic and diagnostic options for Myc-driven hepatic tumours.

| S-EPMC10620125 | biostudies-literature

Protein lysine methyltransferase G9a acts on non-histone targets.

Project description:By methylation of peptide arrays, we determined the specificity profile of the protein methyltransferase G9a. We show that it mostly recognizes an Arg-Lys sequence and that its activity is inhibited by methylation of the arginine residue. Using the specificity profile, we identified new non-histone protein targets of G9a, including CDYL1, WIZ, ACINUS and G9a (automethylation), as well as peptides derived from CSB. We demonstrate potential downstream signaling pathways for methylation of non-histone proteins.

| S-EPMC2696268 | biostudies-literature

Histone H3K9 methyltransferase G9a represses PPAR? expression and adipogenesis.

Project description:PPAR? promotes adipogenesis while Wnt proteins inhibit adipogenesis. However, the mechanisms that control expression of these positive and negative master regulators of adipogenesis remain incompletely understood. By genome-wide histone methylation profiling in preadipocytes, we find that among gene loci encoding adipogenesis regulators, histone methyltransferase (HMT) G9a-mediated repressive epigenetic mark H3K9me2 is selectively enriched on the entire PPAR? locus. H3K9me2 and G9a levels decrease during adipogenesis, which correlates inversely with induction of PPAR?. Removal of H3K9me2 by G9a deletion enhances chromatin opening and binding of the early adipogenic transcription factor C/EBP? to PPAR? promoter, which promotes PPAR? expression. Interestingly, G9a represses PPAR? expression in an HMT activity-dependent manner but facilitates Wnt10a expression independent of its enzymatic activity. Consistently, deletion of G9a or inhibiting G9a HMT activity promotes adipogenesis. Finally, deletion of G9a in mouse adipose tissues increases adipogenic gene expression and tissue weight. Thus, by inhibiting PPAR? expression and facilitating Wnt10a expression, G9a represses adipogenesis.

| S-EPMC3545301 | biostudies-literature

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