scholarly journals DNA Methylation Patterns in the Round Goby Hypothalamus Support an On-The-Spot Decision Scenario for Territorial Behavior

Genes ◽  
2019 ◽  
Vol 10 (3) ◽  
pp. 219 ◽  
Author(s):  
Vincent Somerville ◽  
Michaela Schwaiger ◽  
Philipp E. Hirsch ◽  
Jean-Claude Walser ◽  
Karen Bussmann ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Early Life ◽  
Life Experiences ◽  
Round Goby ◽  
High Growth ◽  
Neogobius Melanostomus ◽  
Epigenetic Mechanism ◽  
Fish Model ◽  
Methylation Patterns ◽  
Reproductive Phenotype

The question as to how early life experiences are stored on a molecular level and affect traits later in life is highly topical in ecology, medicine, and epigenetics. In this study, we use a fish model to investigate whether DNA methylation mediates early life experiences and predetermines a territorial male reproductive phenotype. In fish, adult reproductive phenotypes frequently depend on previous life experiences and are often associated with distinct morphological traits. DNA methylation is an epigenetic mechanism which is both sensitive to environmental conditions and stably inherited across cell divisions. We therefore investigate early life predisposition in the round goby Neogobius melanostomus by growth back-calculations and then study DNA methylation by MBD-Seq in the brain region controlling vertebrate reproductive behavior, the hypothalamus. We find a link between the territorial reproductive phenotype and high growth rates in the first year of life. However, hypothalamic DNA methylation patterns reflect the current behavioral status independently of early life experiences. Together, our data suggest a non-predetermination scenario in the round goby, in which indeterminate males progress to a non-territorial status in the spawning season, and in which some males then assume a specialized territorial phenotype if current conditions are favorable.

scholarly journals DNA methylation patterns in the round goby hypothalamus support an on-the-spot decision scenario for territorial behaviour

2018 ◽  
Author(s):  
Irene Adrian-Kalchhauser ◽  
Vincent Somerville ◽  
Michaela Schwaiger ◽  
Philipp Hirsch ◽  
Karen Bussmann ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Early Life ◽  
Life Experiences ◽  
Round Goby ◽  
High Growth ◽  
Reproductive Behaviour ◽  
Neogobius Melanostomus ◽  
Epigenetic Mechanism ◽  
Methylation Patterns ◽  
Reproductive Phenotype

How early life experiences are stored on a molecular level and affect behavioural phenotypes later in life is not well understood. In fish, reproductive phenotypes are often easily discernible and frequently depend on previous life experiences. DNA methylation is an epigenetic mechanism which is both sensitive to environmental conditions and stable across cell divisions. In this study, we therefore investigate whether DNA methylation mediates early life experiences and predetermines the territorial male reproductive phenotype in the round goby, Neogobius melanostomus. We investigate early life predisposition by growth back-calculations and then study DNA methylation by MBD-Seq in the round goby hypothalamus as the brain region controlling vertebrate reproductive behaviour. We find that the territorial reproductive phenotype is linked to a high growth rate in the first year of life. Hypothalamic DNA methylation patterns, however, reflect the current behavioural status independently of early life experiences. Together, our data suggest a non-predetermination scenario in which indeterminate males progress to a non-territorial status in the spawning season, and in which some males then assume a specialized territorial phenotype if current conditions are favourable.

scholarly journals Gene regulation contributes to explain the impact of early life socioeconomic disadvantage on adult inflammatory levels in two cohort studies

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cristian Carmeli ◽  
Zoltán Kutalik ◽  
Pashupati P. Mishra ◽  
Eleonora Porcu ◽  
Cyrille Delpierre ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Gene Regulation ◽  
Cohort Studies ◽  
Early Life ◽  
Life Experiences ◽  
Socioeconomic Disadvantage ◽  
Mediating Role ◽  
The Impact ◽  
The Relationship

AbstractIndividuals experiencing socioeconomic disadvantage in childhood have a higher rate of inflammation-related diseases decades later. Little is known about the mechanisms linking early life experiences to the functioning of the immune system in adulthood. To address this, we explore the relationship across social-to-biological layers of early life social exposures on levels of adulthood inflammation and the mediating role of gene regulatory mechanisms, epigenetic and transcriptomic profiling from blood, in 2,329 individuals from two European cohort studies. Consistently across both studies, we find transcriptional activity explains a substantive proportion (78% and 26%) of the estimated effect of early life disadvantaged social exposures on levels of adulthood inflammation. Furthermore, we show that mechanisms other than cis DNA methylation may regulate those transcriptional fingerprints. These results further our understanding of social-to-biological transitions by pinpointing the role of gene regulation that cannot fully be explained by differential cis DNA methylation.

scholarly journals The contrasting response to drought and waterlogging is underpinned by divergent DNA methylation programs associated with gene expression in sesame

2018 ◽  
Author(s):  
Komivi Dossa ◽  
Marie Ali Mmadi ◽  
Rong Zhou ◽  
Qi Zhou ◽  
Mei Yang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Abiotic Stresses ◽  
Cytosine Methylation ◽  
De Novo ◽  
Recovery Phase ◽  
Epigenetic Mechanism ◽  
Drought Tolerant ◽  
Sesame Genotypes ◽  
Methylation Patterns

AbstractDNA methylation is a heritable epigenetic mechanism that participates in gene regulation under abiotic stresses in plants. Sesame (Sesamum indicum L.) is typically considered a drought-tolerant crop but highly susceptible to waterlogging, a property attributed to its presumed origin in Africa or India. Understanding DNA methylation patterns in sesame under drought and waterlogging conditions can provide insights into the regulatory mechanisms underlying its contrasting responses to these principal abiotic stresses. Here, we combined Methylation-Sensitive Amplified Polymorphism and transcriptome analyses to profile cytosine methylation patterns, gene expression alteration, and their interplay in drought-tolerant and waterlogging-tolerant sesame genotypes under control, stress and recovery conditions. Our data showed that drought stress strongly induced de novo methylation (DNM) whereas most of the loci were demethylated (DM) during the recovery phase. In contrast, waterlogging decreased the level of methylation under stress but during the recovery phase, both DM and DNM were concomitantly deployed. In both stresses, the differentially expressed genes (DEGs) were highly correlated with the methylation patterns. We observed that DM was associated with the up-regulation of the DEGs while DNM was correlated with the down-regulation of the DEGs. In addition, we sequenced 44 differentially methylated regions of which 90% overlapped with the promoters and coding sequences of the DEGs. Altogether, we demonstrated that sesame has divergent epigenetic programs that respond to drought and waterlogging stresses. Our results also highlighted the possible interplay among DNA methylation and gene expression, which may modulate the contrasting responses to drought and waterlogging in sesame.

scholarly journals On the Use of Blood Samples for Measuring DNA Methylation in Ecological Epigenetic Studies

2020 ◽  
Vol 60 (6) ◽  
pp. 1558-1566 ◽  
Author(s):  
Arild Husby
Keyword(s):  
Dna Methylation ◽  
Phenotypic Variation ◽  
Evolutionary Biology ◽  
Phenotypic Diversity ◽  
Genomic Region ◽  
Epigenetic Mechanism ◽  
Blood Samples ◽  
Reduced Representation ◽  
Bisulfite Treatment ◽  
Methylation Patterns

Synopsis There is increasing interest in understanding the potential for epigenetic factors to contribute to phenotypic diversity in evolutionary biology. One well studied epigenetic mechanism is DNA methylation, the addition of a methyl group to cytosines, which have the potential to alter gene expression depending on the genomic region in which it takes place. Obtaining information about DNA methylation at genome-wide scale has become straightforward with the use of bisulfite treatment in combination with reduced representation or whole-genome sequencing. While it is well recognized that methylation is tissue specific, a frequent limitation for many studies is that sampling-specific tissues may require sacrificing individuals, something which is generally undesirable and sometimes impossible. Instead, information about DNA methylation patterns in the blood is frequently used as a proxy tissue. This can obviously be problematic if methylation patterns in the blood do not reflect that in the relevant tissue. Understanding how, or if, DNA methylation in blood reflect DNA methylation patterns in other tissues is therefore of utmost importance if we are to make inferences about how observed differences in methylation or temporal changes in methylation can contribute to phenotypic variation. The aim of this review is to examine what we know about the potential for using blood samples in ecological epigenetic studies. I briefly outline some methods by which we can measure DNA methylation before I examine studies that have compared DNA methylation patterns across different tissues and, finally, examine how useful blood samples may be for ecological studies of DNA methylation. Ecological epigenetic studies are in their infancy, but it is paramount for the field to move forward to have detailed information about tissue and time dependence relationships in methylation to gain insights into if blood DNA methylation patterns can be a reliable bioindicator for changes in methylation that generate phenotypic variation in ecologically important traits.

scholarly journals Population DNA methylation studies in the Developmental Origins of Health and Disease (DOHaD) framework

2018 ◽  
Vol 10 (3) ◽  
pp. 306-313 ◽  
Author(s):  
J. F. Felix ◽  
C. A. M. Cecil
Keyword(s):  
Dna Methylation ◽  
Health Outcomes ◽  
Early Life ◽  
Later Life ◽  
Epigenetic Mechanism ◽  
Future Research ◽  
Developmental Origins ◽  
Use Of Resources ◽  
Health And Disease

AbstractEpigenetic changes represent a potential mechanism underlying associations of early-life exposures and later life health outcomes. Population-based cohort studies starting in early life are an attractive framework to study the role of such changes. DNA methylation is the most studied epigenetic mechanism in population research. We discuss the application of DNA methylation in early-life population studies, some recent findings, key challenges and recommendations for future research. Studies into DNA methylation within the Developmental Origins of Health and Disease framework generally either explore associations between prenatal exposures and offspring DNA methylation or associations between offspring DNA methylation in early life and later health outcomes. Only a few studies to date have integrated prospective exposure, epigenetic and phenotypic data in order to explicitly test the role of DNA methylation as a potential biological mediator of environmental effects on health outcomes. Population epigenetics is an emerging field which has challenges in terms of methodology and interpretation of the data. Key challenges include tissue specificity, cell type adjustment, issues of power and comparability of findings, genetic influences, and exploring causality and functional consequences. Ongoing studies are working on addressing these issues. Large collaborative efforts of prospective cohorts are emerging, with clear benefits in terms of optimizing power and use of resources, and in advancing methodology. In the future, multidisciplinary approaches, within and beyond longitudinal birth and preconception cohorts will advance this complex, but highly promising, the field of research.

scholarly journals Impact of mothers' early life exposure to low or high folate on progeny outcome and DNA methylation patterns

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Lundi Ly ◽  
Donovan Chan ◽  
Mylène Landry ◽  
Camille Angle ◽  
Josée Martel ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Folic Acid ◽  
Early Life ◽  
Daily Intake ◽  
Oocyte Quality ◽  
Next Generation ◽  
Early Life Exposure ◽  
Generation Progeny ◽  
F2 Generation ◽  
Methylation Patterns

Abstract The dynamic patterning of DNA and histone methylation during oocyte development presents a potentially susceptible time for epigenetic disruption due to early life environmental exposure of future mothers. We investigated whether maternal exposure to folic acid deficient and supplemented diets starting in utero could affect oocytes and cause adverse developmental and epigenetic effects in next generation progeny. Female BALB/c mice (F0) were placed on one of four amino acid defined diets for 4 weeks before pregnancy and throughout gestation and lactation: folic acid control (rodent recommended daily intake; Ctrl), 7-fold folic acid deficient, 10-fold folic acid supplemented or 20-fold folic acid supplemented diets. F1 female pups were weaned onto Ctrl diets, mated to produce the F2 generation and the F2 offspring were examined at E18.5 for developmental and epigenetic abnormalities. Resorption rates were increased and litter sizes decreased amongst F2 E18.5-day litters in the 20-fold folic acid supplemented group. Increases in abnormal embryo outcomes were observed in all three folic acid deficient and supplemented groups. Subtle genome-wide DNA methylation alterations were found in the placentas and brains of F2 offspring in the 7-fold folic acid deficient , 10-fold folic acid supplemented and 20-fold folic acid supplemented groups; in contrast, global and imprinted gene methylation were not affected. The findings show that early life female environmental exposures to both low and high folate prior to oocyte maturation can compromise oocyte quality, adversely affecting offspring of the next generation, in part by altering DNA methylation patterns.

scholarly journals Early life DNA methylation profiles are indicative of age-related transcriptome changes

2019 ◽  
Author(s):  
Niran Hadad ◽  
Dustin R. Masser ◽  
Laura Blanco-Berdugo ◽  
David R. Stanford ◽  
Willard M. Freeman
Keyword(s):  
Dna Methylation ◽  
Early Life ◽  
Functional Outcomes ◽  
Brain Aging ◽  
Epigenetic Modification ◽  
Integrated Analysis ◽  
Epigenetic Variability ◽  
Age Related ◽  
Developmental Origins Of Disease ◽  
Methylation Patterns

AbstractAlterations to cellular and molecular programs with brain aging result in cognitive impairment and susceptibility to neurodegenerative disease. Changes in DNA methylation patterns, an epigenetic modification required for various CNS functions, are observed with aging and can be prevented by anti-aging interventions, but the functional outcomes of altered methylation on transcriptome profiles are poorly understood with brain aging. Integrated analysis of the hippocampal methylome and transcriptome with aging of male and female mice demonstrates that age-related differences in methylation and gene expression are anti-correlated within gene bodies and enhancers, but not promoters. Methylation levels at young age of genes altered with aging are positively associated with age-related expression changes even in the absence of significant changes to methylation with aging, a finding also observed in mouse Alzheimer’s models. DNA methylation patterns established in youth, in combination with other epigenetic marks, are able to predict changes in transcript trajectories with aging. These findings are consistent with the developmental origins of disease hypothesis and indicate that epigenetic variability in early life may explain differences in age-related disease.

scholarly journals TGF-β signaling controls Foxp3 methylation and T reg cell differentiation by modulating Uhrf1 activity

2019 ◽  
Vol 216 (12) ◽  
pp. 2819-2837 ◽  
Author(s):  
Xiang Sun ◽  
Yu Cui ◽  
Haiyun Feng ◽  
Haifeng Liu ◽  
Xiaolong Liu
Keyword(s):  
Dna Methylation ◽  
T Cells ◽  
Cell Differentiation ◽  
Inflammatory Diseases ◽  
Epigenetic Mechanism ◽  
Immune Homeostasis ◽  
Potential Therapeutic Target ◽  
Naive T Cells ◽  
Naïve T Cells ◽  
Methylation Patterns

Regulatory T (T reg) cells are required for the maintenance of immune homeostasis. Both TGF-β signaling and epigenetic modifications are important for Foxp3 induction, but how TGF-β signaling participates in the epigenetic regulation of Foxp3 remains largely unknown. Here we showed that T cell–specific ablation of Uhrf1 resulted in T reg–biased differentiation in TCR-stimulated naive T cells in the absence of TGF-β signaling, and these Foxp3+ T cells had a suppressive function. Adoptive transfer of Uhrf1−/− naive T cells could significantly suppress colitis due to increased iT reg cell generation. Mechanistically, Uhrf1 was induced upon TCR stimulation and participated in the maintenance of DNA methylation patterns of T reg cell–specific genes during cell division, while it was phosphorylated upon TGF-β stimulation and sequestered outside the nucleus, and ultimately underwent proteasome-dependent degradation. Collectively, our study reveals a novel epigenetic mechanism of TGF-β–mediated iT reg cell differentiation by modulating Uhrf1 activity and suggests that Uhrf1 may be a potential therapeutic target in inflammatory diseases for generating stable iT reg cells.

scholarly journals Early-life DNA methylation profiles are indicative of age-related transcriptome changes

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Niran Hadad ◽  
Dustin R. Masser ◽  
Laura Blanco-Berdugo ◽  
David R. Stanford ◽  
Willard M. Freeman
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Early Life ◽  
Brain Aging ◽  
Epigenetic Modification ◽  
Age Related ◽  
Developmental Origins Of Disease ◽  
Altered Gene ◽  
Methylation Patterns ◽  
Relationship Of

Abstract Background Alterations to cellular and molecular programs with brain aging result in cognitive impairment and susceptibility to neurodegenerative disease. Changes in DNA methylation patterns, an epigenetic modification required for various CNS functions are observed with brain aging and can be prevented by anti-aging interventions, but the relationship of altered methylation to gene expression is poorly understood. Results Paired analysis of the hippocampal methylome and transcriptome with aging of male and female mice demonstrates that age-related differences in methylation and gene expression are anti-correlated within gene bodies and enhancers. Altered promoter methylation with aging was found to be generally un-related to altered gene expression. A more striking relationship was found between methylation levels at young age and differential gene expression with aging. Highly methylated gene bodies and promoters in early life were associated with age-related increases in gene expression even in the absence of significant methylation changes with aging. As well, low levels of methylation in early life were correlated to decreased expression with aging. This relationship was also observed in genes altered in two mouse Alzheimer’s models. Conclusion DNA methylation patterns established in youth, in combination with other epigenetic marks, were able to accurately predict changes in transcript trajectories with aging. These findings are consistent with the developmental origins of disease hypothesis and indicate that epigenetic variability in early life may explain differences in aging trajectories and age-related disease.

scholarly journals Dysregulation of Neuronal Genes by Fetal-Neonatal Iron Deficiency Anemia Is Associated with Altered DNA Methylation in the Rat Hippocampus

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1191 ◽  
Author(s):  
Yu-Chin Lien ◽  
David E Condon ◽  
Michael K Georgieff ◽  
Rebecca A Simmons ◽  
Phu V Tran
Keyword(s):  
Dna Methylation ◽  
Iron Deficiency ◽  
Early Life ◽  
Rat Hippocampus ◽  
Epigenetic Mechanism ◽  
Deficiency Anemia ◽  
Gene Dysregulation ◽  
Iron Deficient ◽  
Neuronal Genes

Early-life iron deficiency results in long-term abnormalities in cognitive function and affective behavior in adulthood. In preclinical models, these effects have been associated with long-term dysregulation of key neuronal genes. While limited evidence suggests histone methylation as an epigenetic mechanism underlying gene dysregulation, the role of DNA methylation remains unknown. To determine whether DNA methylation is a potential mechanism by which early-life iron deficiency induces gene dysregulation, we performed whole genome bisulfite sequencing to identify loci with altered DNA methylation in the postnatal day (P) 15 iron-deficient (ID) rat hippocampus, a time point at which the highest level of hippocampal iron deficiency is concurrent with peak iron demand for axonal and dendritic growth. We identified 229 differentially methylated loci and they were mapped within 108 genes. Among them, 63 and 45 genes showed significantly increased and decreased DNA methylation in the P15 ID hippocampus, respectively. To establish a correlation between differentially methylated loci and gene dysregulation, the methylome data were compared to our published P15 hippocampal transcriptome. Both datasets showed alteration of similar functional networks regulating nervous system development and cell-to-cell signaling that are critical for learning and behavior. Collectively, the present findings support a role for DNA methylation in neural gene dysregulation following early-life iron deficiency.

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