Search bioRxiv⌕ Search

Biology subjects

Kimmins, S.

Publications and source records attributed to Kimmins, S..

3 recordsLinked to original sources

Paternal obesity alters the sperm epigenome and is associated with changes in the placental transcriptome and cellular composition

Paternal obesity has been implicated in adult-onset metabolic disease in offspring. However, the molecular mechanisms driving these paternal effects and the developmental processes involved remain poorly understood. One underexplored possibility is the role of paternally driven gene expression in placenta function. To address this, we investigated paternal high-fat diet-induced obesity in relation to sperm epigenetic signatures, the placenta transcriptome and cellular composition. C57BL6/J males were fed either a control or high-fat diet for 10 weeks beginning at 6 weeks of age. Males were timed-mated with control-fed C57BL6/J females to generate pregnancies, followed by collection of sperm, and placentas at embryonic day (E)14.5. Chromatin immunoprecipitation targeting histone H3 lysine 4 tri-methylation (H3K4me3) followed by sequencing (ChIP-seq) was performed on sperm to define obesity-associated changes in enrichment. Paternal obesity corresponded with altered sperm H3K4me3 enrichment at imprinted genes, and at promoters of genes involved in metabolism and development. Notably, sperm altered H3K4me3 was localized at placental enhancers and genes implicated in placental development and function. Bulk RNA-sequencing on placentas detected paternal obesity-induced sex-specific changes in gene expression associated with hypoxic processes such as angiogenesis, nutrient transport and imprinted genes. Paternal obesity was also linked to placenta development; specifically, a deconvolution analysis revealed altered trophoblast cell lineage specification. These findings implicate paternal obesity-effects on placenta development and function as one mechanism underlying offspring metabolic disease. Summary sentencePaternal obesity impacts the sperm epigenome at genes implicated in placenta development and is associated with an altered placenta transcriptome and trophoblast cell lineage specification.

developmental biology↗

Exposure of Greenlandic Inuit and South African VhaVenda men to the persistent DDT metabolite is associated with an altered sperm epigenome at regions implicated in paternal epigenetic transmission and developmental disease - a cross-sectional study

BackgroundThe persistent organochlorine dichlorodiphenyltrichloroethane (DDT) is banned world-wide due to its negative health effects and persistence in the environment. It is exceptionally used as an insecticide for malaria control. Exposure occurs in regions where DDT is applied, as well as in the arctic where its endocrine disrupting metabolite, p,p-dichlorodiphenyldichloroethylene (p,p-DDE) accumulates in marine mammals and fish. DDT and p,p-DDE exposures are linked to birth defects, infertility, cancer, and neurodevelopmental delays. Of particular concern is the potential of DDT use to impact the health of generations to come. Generational effects of toxicant exposures have been described in animal models and implicated germline epigenetic factors. Similar generational effects have been shown in epidemiological studies. Although advances in understanding the molecular mechanisms mediating this epigenetic inheritance have been made, there remain major knowledge gaps in how this occurs in humans. In animal and human models, DNA methylation (DNAme) has been implicated in paternal epigenetic effects. In animal models, histone H3K4 trimethylation (H3K4me3) has been shown to be responsive to the paternal environment and linked with epigenetic transmission to the embryo. Our objectives were to define the associations between p,p-DDE serum levels and alterations in the sperm methylome and H3K4me3 enrichment using next generation sequencing. We aimed to compare regions of epigenomic sensitivity between geographically diverse populations with different routes and levels of exposures, and to identify interactions between altered DNAme and H3K4me3 regions. The potential for p,p-DDE to impact the health of the next generation was explored by examining the functions of the genomic regions impacted, their roles during embryo development, and in health and disease. MethodsIn the Limpopo Province of South Africa, we recruited 247 VhaVenda South African men from 12 villages that either used indoor residual spraying with DDT for malaria control or not. We selected 49 paired blood and semen samples, from men that ranged from 18 to 32 years of age (mean 25 years). Sample inclusion was based on normal sperm counts (> 15 million/ml), normal sperm DNA fragmentation index, and testing a range of p,p-DDE exposure levels (mean 10,462.228 {+/-} 1,792.298 ng/ml). From a total of 193 samples, 47 Greenlandic Inuit blood and semen paired samples were selected from the biobank of the INUENDO cohort. The subjects ranged from 20 to 44 years of age (mean 31 years), were born in Greenland, and all had proven fertility. Sample selection was based on obtaining a range of p,p-DDE exposure levels (mean 870.734 {+/-} 134.030 ng/ml). Here we determined the molecular responses at the level of the sperm epigenome to serum p,p-DDE levels using MethylC-Capture-seq (MCC-seq) and chromatin-immunoprecipitation followed by sequencing (ChIP-seq). We identified genomic regions with altered DNA methylation (DNAme) and differential enrichment of histone H3 lysine 4 trimethylation (H3K4me3) in sperm. We used in silico analyses to discover regions of differential methylation associated with p,p-DDE levels that were predicted to be transmitted and persist in the embryo. ResultsAlterations in DNAme and H3K4me3 enrichment followed dose response-like trends, and we identified overlapping genomic regions with DNAme sensitivities in both populations. Altered DNAme and H3K4me3 in sperm occurred at transposable elements and regulatory regions involved in fertility, disease, development, and neurofunction. A subset of regions with altered sperm DNAme and H3K4me3 were predicted to persist in the pre-implantation embryo and were associated with embryonic gene expression. LimitationsThe samples were collected from remote areas of the world thus sample size is relatively small. The populations differed in the routes of exposure, timing of collection, mean age (mean of 25 versus 31 years of age in South African and Greenlandic populations respectively) and in the timing of p,p-DDE measurement. Moreover, the Greenlandic Inuit men were proven fertile whereas the fertility status of the South African men was unknown. Confounding factors such as other environmental exposures and selection bias cannot be ruled out. ConclusionsThese findings suggest that in men, DDT and p,p-DDE exposure impacts the sperm epigenome in a dose-responsive manner and may negatively impact the health of future generations through epigenetic mechanisms.

genomics↗

Genetic-epigenetic interactions in paternal transgenerational inheritance of metabolic disorders

ObjectiveParental environmental exposures can strongly influence descendant risks for adult disease. How paternal obesity changes the sperm chromatin leading to the acquisition of metabolic disease in offspring remains controversial and ill-defined. The objective of this study was to assess: (1) whether obesity induced by a high-fat diet alters sperm histone methylation; (2) whether paternal obesity can induce metabolic disturbances across generations; (3) whether there could be cumulative damage to the sperm epigenome leading to enhanced metabolic dysfunction in descendants; and (4) whether obesity-sensitive regions associate with embryonic epigenetic and transcriptomic profiles. Using a genetic mouse model of epigenetic inheritance, we investigated the role of histone H3 lysine 4 methylation (H3K4me3) in the paternal transmission of metabolic dysfunction. This transgenic mouse overexpresses the histone demethylase enzyme KDM1A in the developing germline and has an altered sperm epigenome at the level of histone H3K4 methylation. We hypothesized that challenging transgenic sires with a high-fat diet would further erode the sperm epigenome and lead to enhanced metabolic disturbances in the next generations. MethodsTo assess whether paternal obesity can have inter- or transgenerational impacts, and if so, to identify potential mechanisms of this non-genetic inheritance, we used wildtype C57BL/6NCrl and transgenic males with a pre-existing altered sperm epigenome. To induce obesity, sires were fed either a control or high-fat diet (10% or 60% kcal fat, respectively) for 10-12 weeks, then bred to wildtype C57BL/6NCrl female fed a regular diet. F1 and F2 descendants were characterized for metabolic phenotypes by examining the effects of paternal obesity by sex, on body weight, fat mass distribution, the liver transcriptome, intraperitoneal glucose and insulin tolerance tests. To determine whether obesity altered the F0 sperm chromatin, native chromatin immunoprecipitation-sequencing targeting H3K4me3 was performed. To gain insight into mechanisms of paternal transmission, we compared our sperm H3K4me3 profiles with embryonic and placental chromatin states, histone modification and gene expression profiles. ResultsObesity-induced alterations in H3K4me3 occurred at genes implicated in metabolic, inflammatory, and developmental processes. These processes were associated with offspring metabolic dysfunction and corresponded to genes enriched for H3K4me3 in embryos, and overlapped embryonic and placenta gene expression profiles. Transgenerational susceptibility to metabolic disease was only observed when obese F0 had a pre-existing modified sperm epigenome. This coincided with increased H3K4me3 alterations in sperm and more severe phenotypes affecting their offspring. ConclusionsOur data suggest sperm H3K4me3 might serve as a metabolic sensor that connects paternal diet with offspring phenotypes via the placenta. 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. This study highlights the need to further study the connection between the sperm epigenome, placental development and childrens health.

developmental biology↗