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Intergenerational metabolic priming by sperm piRNAs

ABSTRACT: Intergenerational metabolic priming by sperm piRNAs

PROVIDER: PRJNA722018 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14239938.fastq.gz	Fastqsanger.gz
	SRR14239939.fastq.gz	Fastqsanger.gz
	SRR14239940.fastq.gz	Fastqsanger.gz
	SRR14239941.fastq.gz	Fastqsanger.gz
	SRR14239942.fastq.gz	Fastqsanger.gz

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Similar Datasets

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 tsRNAs contribute to intergenerational inheritance of an acquired metabolic disorder

Project description:Increasing evidences indicate diet-induced metabolic disorder could be paternally inherited, but the exact sperm epigenetic carrier remains unclear. Here, in a paternal high-fat diet (HFD) mouse model, we revealed that a highly enriched subset of sperm small RNAs (30-34 nt) that derived from the 5â halves of tRNAs (tsRNAs), exhibit changes in both expression profiles and RNA modifications. Injection of sperm tsRNAs from HFD male but not synthetic tsRNAs lacking RNA modifications, into normal zygotes generated metabolic disorders in the F1 offspring. Injection of HFD sperm tsRNAs derails gene expression in both early embryos and islets of F1 offspring, enriched in metabolic pathways, but unrelated to DNA methylation at CpG-enriched region. Collectively, we uncover sperm tsRNAs as a type of âepigenetic carrierâ that mediate intergenerational inheritance of acquired traits. Mature sperm small-RNA profiles between High-fat-diet (HFD) and Normal-diet (ND) males; Transcriptional profiles of 8-cell embryos and balstocysts that developed from zygotes that injected with sperm RNAs from HFD vs ND males. Transcriptional profiles and RRBS profiles of islets of F1 offsrping that generated from zygotes that injected with sperm RNAs from HFD vs ND males.

2015-12-31 | E-GEOD-75544 | biostudies-arrayexpress

Oocyte piRNAs mediate intergenerational transmission of an acquired metabolic disorder (small RNA sequencing)

Project description:Traditional research has focused on DNA as the molecule that carries heritable information from the parent to the offspring. However, increasing evidence suggests that information beyond the DNA sequence, termed epigenetic information, can also transmit certain information from one generation to the next. Whereas paternal epigenetic germline inheritance has been well elucidated, as the father contributes little more than a sperm cell to the offspring, maternal epigenetic inheritance via gametes remains largely unclear. Here, using an in vitro fertilization system and a micromanipulation strategy, we demonstrate that oocyte piRNAs mediate intergenerational transmission of an acquired metabolic disorder. Changes in the expression profiles of many oocyte piRNAs are observed in a maternal chronic high-fat diet (HFD) mouse model. Injection of the oocyte piRNAs from HFD females into normal zygotes resulted in impaired glucose tolerance and decreased insulin sensitivity in the F1 offspring. A series of genes involved in glucose metabolism and the insulin signaling pathway were differentially expressed in the pancreatic islets of the F1 offspring. Bisulfite genome sequencing of the islets of the F1 offspring revealed changes in cytosine methylation that correlated with the observed gene expression patterns. These data identified oocyte piRNAs as novel carriers of epigenetic information and highlight the importance of long-term maternal health before conception.

2021-05-17 | GSE174504 | GEO

Sperm tsRNAs contribute to intergenerational inheritance of an acquired metabolic disorder

Project description:Increasing evidences indicate diet-induced metabolic disorder could be paternally inherited, but the exact sperm epigenetic carrier remains unclear. Here, in a paternal high-fat diet (HFD) mouse model, we revealed that a highly enriched subset of sperm small RNAs (30-34 nt) that derived from the 5’ halves of tRNAs (tsRNAs), exhibit changes in both expression profiles and RNA modifications. Injection of sperm tsRNAs from HFD male but not synthetic tsRNAs lacking RNA modifications, into normal zygotes generated metabolic disorders in the F1 offspring. Injection of HFD sperm tsRNAs derails gene expression in both early embryos and islets of F1 offspring, enriched in metabolic pathways, but unrelated to DNA methylation at CpG-enriched region. Collectively, we uncover sperm tsRNAs as a type of “epigenetic carrier” that mediate intergenerational inheritance of acquired traits.

2015-12-31 | GSE75544 | 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

Oocyte piRNAs mediate intergenerational transmission of an acquired metabolic disorder (small RNA sequencing)

Project description:Oocyte piRNAs mediate intergenerational transmission of an acquired metabolic disorder (small RNA sequencing)

| PRJNA730307 | ENA

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

| PRJNA548538 | ENA

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

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

| PRJNA548533 | ENA

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]

| PRJNA548280 | ENA

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.

2014-12-04 | E-GEOD-62668 | biostudies-arrayexpress

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