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Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [methylation]

ABSTRACT: Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [methylation]

PROVIDER: PRJNA490451 | ENA |

REPOSITORIES: ENA

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Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [methylation]

Project description:Prenatal stress exposure is associated with the risk for psychiatric disorders later in life. This may be mediated via enhanced exposure to glucocorticoids (GCs), known to impact neurogenesis. We aimed to identify molecular mediators of these effects, focusing on long-lasting epigenetic changes. In a human hippocampal progenitor cell (HPC) line, we assessed the short- and long-term effects of GC exposure during neurogenesis on mRNA expression and DNA methylation (DNAm) profiles. GC exposure induced changes in DNAm at 27,812 CpG sites and in the expression of 3,857 transcripts at FDR ≤ 0.1 and an absolsute change in expression of 1.15. HPC gene expression and GC-affected DNAm profiles were enriched for changes observed during human fetal brain development. Differentially methylated sites (DMSs) with GC exposure clustered into four trajectories over HPC-differentiation, with transient as well as long-lasting DNAm changes. Lasting DMSs mapped to distinct functional pathways and were selectively enriched for poised and bivalent enhancer marks. Lasting DMSs had little correlation with lasting gene expression changes, but were associated with a significantly enhanced transcriptional response to a second acute GC challenge. A significant subset of lasting DMSs was also responsive to an acute GC-challenge in peripheral blood. These tissue-overlapping DMSs were used to compute a poly-epigenetic score that predicted exposure to conditions of excessive prenatal GC in newborn cord blood. Overall, our data suggest that early exposure to GCs can change the set point of future transcriptional responses to stress by inducing lasting DNAm changes. Such altered set points may relate to differential vulnerability to stress exposure later in life.

2019-03-01 | GSE119846 | GEO

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation

Project description:Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation

| PRJNA490449 | ENA

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression_acute]

2019-03-01 | GSE119843 | GEO

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression]

2019-03-01 | GSE119842 | GEO

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression]

Project description:Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression]

| PRJNA490442 | ENA

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression_acute]

Project description:Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation [expression_acute]

| PRJNA490444 | ENA

Glucocorticoid Exposure During Hippocampal Neurogenesis Primes Future Stress Response by Inducing Long-Lasting Changes in DNA Methylation

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

2019-03-01 | GSE119847 | GEO

Glucocorticoid exposure during hippocampal neurogenesis primes future stress response by inducing changes in DNA methylation.

Project description:Prenatal stress exposure is associated with risk for psychiatric disorders later in life. This may be mediated in part via enhanced exposure to glucocorticoids (GCs), which are known to impact neurogenesis. We aimed to identify molecular mediators of these effects, focusing on long-lasting epigenetic changes. In a human hippocampal progenitor cell (HPC) line, we assessed the short- and long-term effects of GC exposure during neurogenesis on messenger RNA (mRNA) expression and DNA methylation (DNAm) profiles. GC exposure induced changes in DNAm at 27,812 CpG dinucleotides and in the expression of 3,857 transcripts (false discovery rate [FDR] ? 0.1 and absolute fold change [FC] expression ? 1.15). HPC expression and GC-affected DNAm profiles were enriched for changes observed during human fetal brain development. Differentially methylated sites (DMSs) with GC exposure clustered into 4 trajectories over HPC differentiation, with transient as well as long-lasting DNAm changes. Lasting DMSs mapped to distinct functional pathways and were selectively enriched for poised and bivalent enhancer marks. Lasting DMSs had little correlation with lasting expression changes but were associated with a significantly enhanced transcriptional response to a second acute GC challenge. A significant subset of lasting DMSs was also responsive to an acute GC challenge in peripheral blood. These tissue-overlapping DMSs were used to compute a polyepigenetic score that predicted exposure to conditions associated with altered prenatal GCs in newborn's cord blood DNA. Overall, our data suggest that early exposure to GCs can change the set point of future transcriptional responses to stress by inducing lasting DNAm changes. Such altered set points may relate to differential vulnerability to stress exposure later in life.

| S-EPMC7519233 | biostudies-literature

Systemic stem cell activation following amputation primes distant appendages for future regeneration events in axolotl

Project description:Systemic stem cell activation following amputation primes distant appendages for future regeneration events in axolotl

| PRJNA791634 | ENA

Allelic chromatin structure primes imprinted expression of Kcnk9 during neurogenesis

Project description:Differences in chromatin state inherited from the parental gametes influence the regulation of maternal and paternal alleles in offspring. This phenomenon, known as genomic imprinting, results in genes preferentially transcribed from one parental allele. While local epigenetic factors such as DNA methylation are known to be important for the establishment of imprinted gene expression, less is known about the mechanisms by which differentially methylated regions (DMRs) lead to differences in allelic expression across broad stretches of chromatin. Allele-specific higher-order chromatin structure has been observed at multiple imprinted loci, consistent with the observation of allelic binding of the chromatin-organizing factor CTCF at multiple DMRs. However, whether allelic chromatin structure impacts allelic gene expression is not known for most imprinted loci. Here we characterize the mechanisms underlying brain-specific imprinted expression of the Peg13-Kcnk9 locus, an imprinted region associated with intellectual disability. We performed region capture Hi-C on mouse brain from reciprocal hybrid crosses and found imprinted higher-order chromatin structure caused by the allelic binding of CTCF to the Peg13 DMR. Using an in vitro neuron differentiation system, we show that on the maternal allele, an enhancer-promoter contact formed early in development primes the brain-specific potassium leak channel Kcnk9 for maternal expression prior to neurogenesis. In contrast, this enhancer-promoter contact is blocked by CTCF on the paternal allele, preventing paternal Kcnk9 activation. This work provides a high-resolution map of imprinted chromatin structure and demonstrates that chromatin state established in early development can promote imprinted expression upon differentiation.

2023-08-07 | GSE202251 | GEO

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