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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE132612 | GEO | 2019/06/13

REPOSITORIES: GEO

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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 [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

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

2019-06-13 | GSE132613 | 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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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.

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Intergenerational programming of hepatic xenobiotic response by paternal Nicotine exposure

Project description:Although it is increasingly accepted that some paternal environmental conditions can influence phenotypes in future generations, it generally remains unclear whether the phenotypes induced in offspring represent specific responses to particular aspects of the paternal exposure history, or whether they represent a more generic response to paternal “quality of life”. To establish a paternal effect model based on a known ligand-receptor interaction and thereby enable pharmacological interrogation of the specificity of the offspring response, we explored the effects of paternal nicotine administration on offspring phenotype in mouse. We show that chronic paternal exposure to nicotine prior to reproduction induced a broad protective response to multiple xenobiotics in the next generation. This effect manifested as increased survival following an injection of toxic levels of either nicotine or of cocaine, was specific to male offspring, and was only observed after offspring were first acclimated to sublethal doses of nicotine or cocaine. Mechanistically, the reprogrammed state was characterized by enhanced clearance of nicotine in drug-acclimated animals, accompanied by hepatic upregulation of genes involved in xenobiotic metabolism. Surprisingly, this protective effect could also be induced by paternal exposure to a nicotinic receptor antagonist as well as to nicotine, suggesting that paternal xenobiotic exposure, rather than nicotinic receptor signaling, is likely to be responsible for programming of offspring drug resistance. Taken together, our data show that paternal drug exposure can induce a protective phenotype in offspring by enhancing metabolic tolerance to xenobiotics in the environment.

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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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Paternal diet defines offspring chromatin state and intergenerational obesity.

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Intergenerational transmission of paternal trauma among US Civil War ex-POWs.

Project description:We study whether paternal trauma is transmitted to the children of survivors of Confederate prisoner of war (POW) camps during the US Civil War (1861-1865) to affect their longevity at older ages, the mechanisms behind this transmission, and the reversibility of this transmission. We examine children born after the war who survived to age 45, comparing children whose fathers were non-POW veterans and ex-POWs imprisoned in very different camp conditions. We also compare children born before and after the war within the same family by paternal ex-POW status. The sons of ex-POWs imprisoned when camp conditions were at their worst were 1.11 times more likely to die than the sons of non-POWs and 1.09 times more likely to die than the sons of ex-POWs when camp conditions were better. Paternal ex-POW status had no impact on daughters. Among sons born in the fourth quarter, when maternal in utero nutrition was adequate, there was no impact of paternal ex-POW status. In contrast, among sons born in the second quarter, when maternal nutrition was inadequate, the sons of ex-POWs who experienced severe hardship were 1.2 times more likely to die than the sons of non-POWs and ex-POWs who fared better in captivity. Socioeconomic effects, family structure, father-specific survival traits, and maternal effects, including quality of paternal marriages, cannot explain our findings. While we cannot rule out fully psychological or cultural effects, our findings are most consistent with an epigenetic explanation.

| S-EPMC6217388 | biostudies-literature

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