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Synchrony and asynchrony between an epigenetic clock and developmental timing [EPIC array]

ABSTRACT: Synchrony and asynchrony between an epigenetic clock and developmental timing [EPIC array]

PROVIDER: PRJNA512519 | ENA |

REPOSITORIES: ENA

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Synchrony and asynchrony between an epigenetic clock and developmental timing

Project description:Synchrony and asynchrony between an epigenetic clock and developmental timing

| PRJNA512517 | ENA

Synchrony and asynchrony between an epigenetic clock and developmental timing [RNA-Seq]

Project description:Synchrony and asynchrony between an epigenetic clock and developmental timing [RNA-Seq]

| PRJNA511410 | ENA

Synchrony and asynchrony between an epigenetic clock and developmental timing [450K array]

Project description:Synchrony and asynchrony between an epigenetic clock and developmental timing [450K array]

| PRJNA512520 | ENA

Synchrony and asynchrony between an epigenetic clock and developmental timing [EPIC array]

Project description:Genome wide DNA methylation profiling of human fetal retina samples. The Illumina Infinium DNA methylation Beadchip was used to obtain DNA methylation profiles in human fetal retina samples that were cultured in different ways. To better undrestand the relationship between developmental stage and epigenetic age (measured by the Horvath clock based on 353 CpGs as detailed in pubmed identifier: 24138928), we analyzed the highly regular sequence of developmental stage in the human neural retina. Findings: epigenetic age of fetal retina is highly correlated with chronological age. We find that epigenetic aging progresses normally in vitro. The correlation is retained in stem cell derived organoids but is accelerated in individuals with Down syndrome.

2020-03-12 | GSE124568 | GEO

Synchrony and asynchrony between an epigenetic clock and developmental timing [450K array]

2020-03-12 | GSE124567 | GEO

Synchrony and asynchrony between an epigenetic clock and developmental timing [RNA-Seq]

Project description:Epigenetic changes have been used to estimate chronological age across the lifespan, and some studies suggest that epigenetic "aging" clocks may already operate in developing tissue. To better understand the relationship between developmental stage and epigenetic age, we utilized the highly regular sequence of development found in the mammalian neural retina and a well-established epigenetic aging clock based on DNA methylation. Our results demonstrate that the epigenetic age of fetal retina is highly correlated with chronological age. We further establish that epigenetic aging progresses normally in vitro, suggesting that epigenetic aging is a property of individual tissues. This correlation is also retained in stem cell-derived retinal organoids, but is accelerated in individuals with Down's syndrome, a progeroid-like condition. Overall, our results suggest that epigenetic aging begins as early as a few weeks post-conception, in fetal tissues, and the mechanisms underlying the phenomenon of epigenetic aging might be studied in developing organs.

2021-01-21 | GSE124252 | GEO

Synchrony and asynchrony between an epigenetic clock and developmental timing.

Project description:Epigenetic changes have been used to estimate chronological age across the lifespan, and some studies suggest that epigenetic "aging" clocks may already operate in developing tissue. To better understand the relationship between developmental stage and epigenetic age, we utilized the highly regular sequence of development found in the mammalian neural retina and a well-established epigenetic aging clock based on DNA methylation. Our results demonstrate that the epigenetic age of fetal retina is highly correlated with chronological age. We further establish that epigenetic aging progresses normally in vitro, suggesting that epigenetic aging is a property of individual tissues. This correlation is also retained in stem cell-derived retinal organoids, but is accelerated in individuals with Down syndrome, a progeroid-like condition. Overall, our results suggest that epigenetic aging begins as early as a few weeks post-conception, in fetal tissues, and the mechanisms underlying the phenomenon of epigenetic aging might be studied in developing organs.

| S-EPMC6403397 | biostudies-literature

Synchrony and asynchrony between an epigenetic clock and developmental timing

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

2020-03-12 | GSE124569 | GEO

Dopamine and GPCR-mediated modulation of DN1 clock neurons gates the circadian timing of sleep

Project description:The metronome-like circadian regulation of sleep timing must still adapt to an uncertain environment. Recent studies in Drosophila indicate that neuromodulation not only plays a key role in clock neuron synchronization but also affects interactions between the clock network and brain sleep centers. We show here that the targets of neuromodulators, G-Protein Coupled Receptors (GPCRs), are highly enriched in the fly brain circadian clock network. Single cell sequencing indicates that they are not only enriched, but they are also differentially expressed and contribute to clock neuron identity. We generated a comprehensive guide library to mutagenize individual GPCRs in specific neurons and verified the strategy by introducing a targeted sequencing approach. Combined with a behavioral screen, the mutagenesis strategy revealed a novel role of dopamine in sleep regulation by identifying two dopamine receptors and a clock neuron subpopulation that gate the timing of sleep.

2022-05-09 | GSE202407 | GEO

Allele specific timing of replication

Project description:We have characterized allele-specific regulation of replication in human cultured primary basophilic erythroblasts using TimEX-seq. We show that in most of the genome the timing of replication of the two chromosome homologs is robustly and tightly regulated since the two alleles replicate almost at the same time. We also show that small genetic differences such as SNPs and indels do not affect replication timing. We identify two major causes of replication asynchrony: the presence of large structural variants and parental imprinting. Both are associated with the formation of asynchronously replicated domains that can reach several megabases in size. We also report that replication timing domains have a previously undetected fine structure.

2014-05-01 | GSE50977 | GEO

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