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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE132613 | GEO | 2019/06/13

REPOSITORIES: GEO

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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 [MeDIP-Seq]

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

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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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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

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

Project description:The discovery of RNAs (for example, messenger RNAs, non-coding RNAs) in sperm has opened the possibility that sperm may function by delivering additional paternal information aside from solely providing the DNA 1 . 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-induced metabolic disorders to offspring. Dnmt2 deletion prevented the elevation of RNA modifications (m5C, m2G) in sperm 30-40?nt RNA fractions that are induced by a high-fat diet. Also, Dnmt2 deletion altered the sperm small RNA expression profile, including levels of tRNA-derived small RNAs and rRNA-derived small RNAs, 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.

| S-EPMC5926820 | biostudies-literature

Angiogenin mediates paternal inflammation-induced metabolic disorders in offspring through sperm tsRNAs.

Project description:Paternal environmental inputs can influence various phenotypes in offspring, presenting tremendous implications for basic biology and public health and policy. However, which signals function as a nexus to transmit paternal environmental inputs to offspring remains unclear. Here we show that offspring of fathers with inflammation exhibit metabolic disorders including glucose intolerance and obesity. Deletion of a mouse tRNA RNase, Angiogenin (Ang), abolished paternal inflammation-induced metabolic disorders in offspring. Additionally, Ang deletion prevented the inflammation-induced alteration of 5'-tRNA-derived small RNAs (5'-tsRNAs) expression profile in sperm, which might be essential in composing a sperm RNA 'coding signature' that is needed for paternal epigenetic memory. Microinjection of sperm 30-40 nt RNA fractions (predominantly 5'-tsRNAs) from inflammatory Ang+/+ males but not Ang-/- males resulted in metabolic disorders in the resultant offspring. Moreover, zygotic injection with synthetic 5'-tsRNAs which increased in inflammatory mouse sperm and decreased by Ang deletion partially resembled paternal inflammation-induced metabolic disorders in offspring. Together, our findings demonstrate that Ang-mediated biogenesis of 5'-tsRNAs in sperm contributes to paternal inflammation-induced metabolic disorders in offspring.

| S-EPMC8630171 | biostudies-literature

Intergenerational Transmission of Paternal Epigenetic Marks: Mechanisms Influencing Susceptibility to Post-Concussion Symptomology in a Rodent Model.

Project description:Epigenetic transmission of phenotypic variance has been linked to paternal experiences prior to conception and during perinatal development. Previous reports indicate that paternal experiences increase phenotypic heterogeneity and may contribute to offspring susceptibility to post-concussive symptomology. This study sought to determine if epigenetic tags, specifically DNA methylation of promoter regions, are transmitted from rodent fathers to their sons. Using MethyLight, promoter methylation of specific genes involved in recovery from concussion and brain plasticity were analyzed in sperm and brain tissue. Promoter methylation in sperm differed based on paternal experience. Differences in methylation were often identified in both the sperm and brain tissue obtained from their sons, demonstrating transmission of epigenetic tags. For certain genes, methylation in the sperm was altered following a concussion suggesting that a history of brain injury may influence paternal transmission of traits. As telomere length is paternally inherited and linked to neurological health, this study examined paternally derived differences in telomere length, in both sperm and brain. Telomere length was consistent between fathers and their sons, and between brain and sperm, with the exception of the older fathers. Older fathers exhibited increased sperm telomere length, which was not evident in sperm or brain of their sons.

| S-EPMC5541091 | biostudies-other

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

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