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Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration [MeDIP-Seq]

ABSTRACT: Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration [MeDIP-Seq]

PROVIDER: PRJNA548533 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9282935_1.fastq.gz	Fastqsanger.gz
	SRR9282935_2.fastq.gz	Fastqsanger.gz
	SRR9282936_1.fastq.gz	Fastqsanger.gz
	SRR9282936_2.fastq.gz	Fastqsanger.gz
	SRR9282937_1.fastq.gz	Fastqsanger.gz

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Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration [MeDIP-Seq]

Project description:We using a mouse model of paternal famine to simulate famine, our data show that paternal famine increases the susceptibility to metabolic disease in offspring through gametic epigenetic alterations.

2019-06-13 | GSE132612 | GEO

Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration [RNA-Seq]

Project description:We used a mouse model of paternal famine to simulate famine, our data show that paternal famine increases the susceptibility to metabolic disease in offspring through gametic epigenetic alterations.

2019-06-12 | GSE132521 | GEO

Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration

Project description:Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration

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Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration [RNA-Seq]

Project description:Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration [RNA-Seq]

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Paternal overdiet drives intergenerational transmission of metabolic disorders through sperm epigenetic alteration

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

2019-06-13 | GSE132613 | GEO

Dnmt2 mediates intergenerational transmission of paternally acquired metabolic disorders through sperm small non-coding RNAs

Project description:The discovery of RNAs (e.g. mRNAs, non-coding RNAs) in sperm has opened the possibility that sperm may function in delivering additional paternal information aside from solely providing the DNA1. Increasing evidence now suggests that sperm small non-coding RNAs (sncRNAs) can mediate intergenerational transmission of paternally acquired phenotypes, including mental stress2, 3 and metabolic disorders4-6. How sperm sncRNAs encode paternal information remains unclear, but the mechanism may involve RNA modifications. Here we show that deletion of a mouse tRNA methyltransferase, DNMT2, abolished sperm sncRNA-mediated transmission of high-fat diet (HFD)-induced metabolic disorders to offspring. Dnmt2 deletion prevented the elevation of RNA modifications (m5C, m2G) in sperm 30-40nt RNA fractions that are induced by HFD. Also, Dnmt2 deletion altered the sperm small RNA expression profile, including levels of tRNA-derived small RNAs (tsRNAs) and rRNA-derived small RNAs (rsRNA-28S), which might be essential in composing a sperm RNA ‘coding signature’ that is needed for paternal epigenetic memory. Finally, we show that Dnmt2-mediated m5C contributes to the secondary structure and biological properties of sncRNAs, implicating sperm RNA modifications as an additional layer of paternal hereditary information.

2018-03-06 | GSE97645 | GEO

MeDIP-seq of ICR mouse sperm with different combinations of in utero undernutrition and postnatal undernutrition

Project description:Maternal caloric restriction during the last week of gestation resulted in low birth weight (LBW) and increased risk of LBW-associated metabolic diseases in adult life. The metabolic phenotypes transmitted to F2 generation by paternal manner without additional altered nutrition. To investigate the mechanism of this intergenerational inheritance, two Cohorts were exposed to different magnitudes of undernutrition both in utero during the last week of gestation and/or postnatal until weaning. We performed MeDIP-seq on the genomic DNA from sperm collected from these mice.

2024-08-25 | E-MTAB-9567 | biostudies-arrayexpress

Paternal diet defines offspring chromatin state and intergenerational obesity.

Project description:The global rise in obesity has revitalized a search to understand genetic, and in particular, epigenetic factors underlying the disease. We present a Drosophila model of paternal-diet-induced Inter-Generational Metabolic Reprogramming (IGMR) and identify genes required for its encoding in offspring. Intriguingly, we find that as little as two days of dietary intervention in fathers elicits obesity in offspring. Paternal sugar acts as a physiological suppressor of variegation, de-silencing chromatin state-defined transcriptional units in both mature sperm and in offspring embryos. We identify requirements for H3K9/K27me3 dependent reprogramming of metabolic genes in two distinct germline and zygotic windows. Critically, we find evidence that a similar system regulates obesity-susceptibility and phenotype variation in mice and humans. The findings provide insight into the mechanisms underlying intergenerational metabolic reprogramming and carry profound implications for our understanding of phenotypic variation and evolution. RNA-seq on Drosophila embryos and sperm samples fed medium and high sugar.

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Intergenerational metabolic priming by sperm piRNAs

Project description:Preconception parental environment can reproducibly program offspring phenotype without altering the DNA sequence, yet the mechanisms underpinning this ‘epigenetic inheritance’ remains elusive. Here, we demonstrate the existence of an intact piRNA-pathway in mature Drosophila sperm and show that pathway modulation alters offspring gene transcription in a sequence-specific manner. We map a dynamic small RNA content in developing sperm and find that the mature sperm carry a highly distinct small RNA cargo. By biochemical pulldown, we identify a small RNA subset bound directly to piwi protein. And, we show that piRNA-pathway controlled sperm small RNAs are linked to target gene repression in offspring. Critically, we find that full piRNA-pathway dosage is necessary for the intergenerational metabolic and transcriptional reprogramming events triggered by high paternal dietary sugar. These data provide a direct link between regulation of endogenous mature sperm small RNAs and transcriptional programming of complementary sequences in offspring. Thus, we identify a novel mediator of paternal intergenerational epigenetic inheritance.

2022-01-01 | GSE172107 | GEO

Sperm transcriptional state associated with paternal transmission of stress phenotypes

Project description:Paternal stress can induce long-lasting changes in germ cells potentially propagating heritable changes across generations. To date, no studies have investigated differences in transmission patterns between stress-resilient and -susceptible mice. We tested the hypothesis that transcriptional alterations in sperm during chronic social defeat stress (CSDS) transmit increased susceptibility to stress phenotypes to the next generation. We demonstrate differences in offspring from stressed fathers that depend upon paternal category (resilient vs susceptible) and offspring sex. Importantly, artificial insemination reveals that sperm mediates some of the behavioral phenotypes seen in offspring. Using RNA-sequencing we report substantial and distinct changes in the transcriptomic profiles of sperm following CSDS in susceptible vs resilient fathers, with alterations in long noncoding RNAs (lncRNAs) predominating especially in susceptibility. Correlation analysis revealed that these alterations were accompanied by a loss of regulation of protein-coding genes by lncRNAs in sperm of susceptible males. We also identify several co-expression gene modules that are enriched in differentially expressed genes in sperm from either resilient or susceptible fathers. Taken together, these studies advance our understanding of intergenerational epigenetic transmission of behavioral experience.

2024-05-20 | GSE174780 | GEO

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