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Acquired paternal inheritance fatty liver transcriptomes induced by high-fat diet

ABSTRACT: Acquired paternal inheritance fatty liver transcriptomes induced by high-fat diet

OTHER RELATED OMICS DATASETS IN: GSE111909

PROVIDER: PRJNA438519 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6844900_1.fastq.gz	Fastqsanger.gz
	SRR6844900_2.fastq.gz	Fastqsanger.gz
	SRR6844895_1.fastq.gz	Fastqsanger.gz
	SRR6844895_2.fastq.gz	Fastqsanger.gz
	SRR6844896_1.fastq.gz	Fastqsanger.gz

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Acquired paternal inheritance fatty liver transcriptomes induced by high-fat diet

Project description:Many acquired traits related to fat metabolism are inherited, and nutritional factors can induce fatty liver in chickens. We found that the paternal fatty livers induced by high-fat diet in Jingxing-Huang chickens were inherited, but the molecular mechanisms of inherited fatty liver in chickens are far from clear. The goals of this study are to compare liver transcriptome profiling (RNA-seq) in F1 generation to screen candidate genes for acquired fatty liver. Compared to birds without fatty liver in the control group, the paternal group exhibited altered hepatic gene expression profiles, including up-regulation of several key genes involved in fatty acid metabolism, lipid metabolism and glucose metabolism (ACACA, FASN, SCD, ACSL5, FADS2, FABP1, APOA4 and ME1). This study uniquely revealed that acquired fatty liver in cocks can be inherited. The hepatic gene expression profiles were altered in chickens with the inherited phenotype of acquired paternal fatty liver and several genes could be candidate biomarkers.

2018-04-09 | GSE111909 | GEO

A membrane-associated condensate ensures paternal epigenetic inheritance in C. elegans

Project description:Transgenerational epigenetic inheritance (TEI) describes the transmission of gene-regulatory information across generations without altering DNA sequences. TEI allows priming of offspring towards changing environmental conditions and plays a role in the maintenance of gene silencing of selfish genetic elements like transposons. Small regulatory RNAs are well known to act in TEI, and can be transmitted via the male. Such inheritance via sperm requires dedicated mechanisms, as much of the cellular content is extruded during spermatogenesis. We identify a phase separation-based mechanism, which couples the paternal inheritance of a specific small RNA-bound silencing factor via S-palmitoylation to the transport of membranous organelles. Our findings uncover a thus far unknown paternal TEI mechanism, and describe a novel mode of transport of phase-separated condensates.

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Project description:PRC2 mediates paternal epigenetic inheritance

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PRC2 mediated paternal epigenetic inheritance

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Paternal chronic folate supplementation induced transgenerational inheritance of acquired developmental and metabolic changes in chickens

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Polycomb protein SCML2 mediates paternal epigenetic inheritance through sperm chromatin

Project description:Sperm chromatin retains small amounts of histones, and the chromatin states of sperm mirror gene expression programs of the next generation. It remains largely unknown how paternal epigenetic information is transmitted through sperm chromatin. Here we developed a novel mouse model of paternal epigenetic inheritance in which deposition of Polycomb repressive complex 2 (PRC2) mediated-repressive H3K27me3 is attenuated in the paternal germline. By applying modified methods of assisted reproductive technology, we rescued infertility of mice absent of Polycomb protein SCML2, which is the regulator of germline gene expression through the establishment of H3K27me3 on bivalent promoters with other active marks H3K4me2/3. In F1 males of Scml2-knockout mice, which has wild-type genotype, gene expression is dysregulated in the male germline during spermiogenesis. These dysregulated genes are targets of SCML2-mediated H3K27me3 in mature sperm. Thus, SCML2 mediates intergenerational inheritance of paternal epigenetic information through the regulation of sperm chromatin.

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Transgenerational inheritance of acquired memory and epigenetic imprints through maternal gametes

Project description:Transgenerational inheritance of acquired traits/characteristics from ancestors is believed to play important roles in evolution, as well as health problems/symptoms not due to “classical genetic inheritance”. However, the central enigma, such as how the acquired transgenerational characteristics are developed, and how the acquired traits are transmitted from generations to generations of offspring, largely remained veiled. In this study, we used C elegans as a model system and provide evidence that the dynamic of H3K27me3 as a hallmark and regulator for the gut-mediated transgenerational inheritance of acquired traits. Further, we demonstrate that yolk proteins guide the establishment of the acquired epigenetic imprints in soma, as well as determines the transgenerational inheritance of epigenetic imprints and subsequent acquired behavior in offspring by maternal provision. Taken together, our findings support that yolk proteins both function as a systemic “non-nuclear factor” for establishing the somatic epigenetic imprints and as a “cargo” to transmit acquired epigenetic information to the subsequent generations through oocytes.

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Project description:Parental environmental exposures can strongly influence descendant risks for adult disease. Metabolic disorders arise from the intersection of environmental and genetic risk factors, with epigenetic inheritance being at the center of the familial cycle of transgenerational disease. How paternal high-fat diet changes the sperm chromatin leading to the acquisition of metabolic disease in offspring remains controversial and ill-defined. Using a genetic model of epigenetic inheritance, we investigated the role of histone H3 lysine 4 methylation (H3K4me3) in the paternal transmission of metabolic dysfunction. We show that obesity-induced alterations in sperm H3K4me3 associated with offspring phenotypes and corresponded to embryonic and placental chromatin profiles and gene expression. Transgenerational susceptibility to metabolic disease was only observed when grandsires had a pre-existing genetic predisposition to metabolic dysfunction that was associated with enhanced alterations to sperm H3K4me3. This non-DNA based knowledge of inheritance has the potential to improve our understanding of how environment shapes heritability and may lead to novel routes for the prevention of disease.

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