@misc{TeifCherstvy2016, author = {Teif, Vladimir B. and Cherstvy, Andrey G.}, title = {Chromatin and epigenetics: current biophysical views}, series = {AIMS biophysics}, volume = {3}, journal = {AIMS biophysics}, publisher = {American Institute of Mathematical Sciences}, address = {Springfield}, issn = {2377-9098}, doi = {10.3934/biophy.2016.1.88}, pages = {88 -- 98}, year = {2016}, abstract = {Recent advances in high-throughput sequencing experiments and their theoretical descriptions have determined fast dynamics of the "chromatin and epigenetics" field, with new concepts appearing at high rate. This field includes but is not limited to the study of DNA-protein-RNA interactions, chromatin packing properties at different scales, regulation of gene expression and protein trafficking in the cell nucleus, binding site search in the crowded chromatin environment and modulation of physical interactions by covalent chemical modifications of the binding partners. The current special issue does not pretend for the full coverage of the field, but it rather aims to capture its development and provide a snapshot of the most recent concepts and approaches. Eighteen open-access articles comprising this issue provide a delicate balance between current theoretical and experimental biophysical approaches to uncover chromatin structure and understand epigenetic regulation, allowing free flow of new ideas and preliminary results.}, language = {en} } @misc{WeyrichJeschekSchrapersetal.2018, author = {Weyrich, Alexandra and Jeschek, Marie and Schrapers, Katharina T. and Lenz, Dorina and Chung, Tzu Hung and Ruebensam, Kathrin and Yasar, Sermin and Schneemann, Markus and Ortmann, Sylvia and Jewgenow, Katarina and Fickel, J{\"o}rns}, title = {Diet changes alter paternally inherited epigenetic pattern in male Wild guinea pigs}, series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, number = {1065}, issn = {1866-8372}, doi = {10.25932/publishup-46003}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-460031}, pages = {14}, year = {2018}, abstract = {Epigenetic modifications, of which DNA methylation is the most stable, are a mechanism conveying environmental information to subsequent generations via parental germ lines. The paternal contribution to adaptive processes in the offspring might be crucial, but has been widely neglected in comparison to the maternal one. To address the paternal impact on the offspring's adaptability to changes in diet composition, we investigated if low protein diet (LPD) in F0 males caused epigenetic alterations in their subsequently sired sons. We therefore fed F0 male Wild guinea pigs with a diet lowered in protein content (LPD) and investigated DNA methylation in sons sired before and after their father's LPD treatment in both, liver and testis tissues. Our results point to a 'heritable epigenetic response' of the sons to the fathers' dietary change. Because we detected methylation changes also in the testis tissue, they are likely to be transmitted to the F2 generation. Gene-network analyses of differentially methylated genes in liver identified main metabolic pathways indicating a metabolic reprogramming ('metabolic shift'). Epigenetic mechanisms, allowing an immediate and inherited adaptation may thus be important for the survival of species in the context of a persistently changing environment, such as climate change.}, language = {en} } @article{WeyrichJeschekSchrapersetal.2018, author = {Weyrich, Alexandra and Jeschek, Marie and Schrapers, Katharina T. and Lenz, Dorina and Chung, Tzu Hung and Ruebensam, Kathrin and Yasar, Sermin and Schneemann, Markus and Ortmann, Sylvia and Jewgenow, Katarina and Fickel, J{\"o}rns}, title = {Diet changes alter paternally inherited epigenetic pattern in male Wild guinea pigs}, series = {Environmental Epigenetics}, volume = {4}, journal = {Environmental Epigenetics}, number = {2}, publisher = {Oxford Univ. Press}, address = {Oxford}, issn = {2058-5888}, doi = {10.1093/eep/dvy011}, pages = {12}, year = {2018}, abstract = {Epigenetic modifications, of which DNA methylation is the most stable, are a mechanism conveying environmental information to subsequent generations via parental germ lines. The paternal contribution to adaptive processes in the offspring might be crucial, but has been widely neglected in comparison to the maternal one. To address the paternal impact on the offspring's adaptability to changes in diet composition, we investigated if low protein diet (LPD) in F0 males caused epigenetic alterations in their subsequently sired sons. We therefore fed F0 male Wild guinea pigs with a diet lowered in protein content (LPD) and investigated DNA methylation in sons sired before and after their father's LPD treatment in both, liver and testis tissues. Our results point to a 'heritable epigenetic response' of the sons to the fathers' dietary change. Because we detected methylation changes also in the testis tissue, they are likely to be transmitted to the F2 generation. Gene-network analyses of differentially methylated genes in liver identified main metabolic pathways indicating a metabolic reprogramming ('metabolic shift'). Epigenetic mechanisms, allowing an immediate and inherited adaptation may thus be important for the survival of species in the context of a persistently changing environment, such as climate change.}, language = {en} } @article{PutraReichetzederMeixneretal.2017, author = {Putra, Sulistyo E. Dwi and Reichetzeder, Christoph and Meixner, Martin and Liere, Karsten and Slowinski, Torsten and Hocher, Berthold}, title = {DNA methylation of the glucocorticoid receptor gene promoter in the placenta is associated with blood pressure regulation in human pregnancy}, series = {Journal of hypertension}, volume = {35}, journal = {Journal of hypertension}, publisher = {Lippincott Williams \& Wilkins}, address = {Philadelphia}, issn = {0263-6352}, doi = {10.1097/HJH.0000000000001450}, pages = {2276 -- 2286}, year = {2017}, abstract = {Background: Blood pressure (BP) regulation during pregnancy is influenced by hormones of placental origin. It was shown that the glucocorticoid system is altered in hypertensive pregnancy disorders such as preeclampsia. Epigenetic mechanism might influence the activity of genes involved in placental hormone/hormone receptor synthesis/action during pregnancy. Method: In the current study, we analyzed the association of 50-C-phosphate-G-30 (CpG) site methylation of different glucocorticoid receptor gene (NR3C1) promoter regions with BP during pregnancy. The study was performed as a nested case-control study (n = 80) out of 1045 mother/ child pairs from the Berlin Birth Cohort. Placental DNA was extracted and bisulfite converted. Nested PCR products from six NR3C1 proximal promoter regions [glucocorticoid receptor gene promotor region B (GR-1B), C (GR-1C), D (GR-1D), E (GR-1E), F (GR-1F), and H (GR-1H)] were analyzed by next generation sequencing. Results: NR3C1 promoter regions GR-1D and GR-1E had a much higher degree of DNA methylation as compared to GR-1B, GR-1F or GR-1H when analyzing the entire study population. Comparison of placental NR3C1 CpG site methylation among hypotensive, normotensive and hypertensive mothers revealed several differently methylated CpG sites in the GR-1F promoter region only. Both hypertension and hypotension were associated with increased DNA methylation of GR-1F CpG sites. These associations were independent of confounding factors, such as family history of hypertension, smoking status before pregnancy and prepregnancy BMI. Assessment of placental glucocorticoid receptor expression by western blot showed that observed DNA methylation differences were not associated with altered levels of placental glucocorticoid receptor expression. However, correlation matrices of all NR3C1 proximal promoter regions demonstrated different correlation patterns of intraregional and interregional DNA methylation in the three BP groups, putatively indicating altered transcriptional control of glucocorticoid receptor isoforms. Conclusion: Our study provides evidence of an independent association between placental NR3C1 proximal promoter methylation and maternal BP. Furthermore, we observed different patterns of NR3C1 promoter methylation in normotensive, hypertensive and hypotensive pregnancy.}, language = {en} } @article{WeyrichLenzFickel2018, author = {Weyrich, Alexandra and Lenz, Dorina and Fickel, J{\"o}rns}, title = {Environmental Change-Dependent Inherited Epigenetic Response}, series = {GENES}, volume = {10}, journal = {GENES}, number = {1}, publisher = {MDPI}, address = {Basel}, issn = {2073-4425}, doi = {10.3390/genes10010004}, pages = {15}, year = {2018}, abstract = {Epigenetic modifications are a mechanism conveying environmental information to subsequent generations via parental germ lines. Research on epigenetic responses to environmental changes in wild mammals has been widely neglected, as well as studies that compare responses to changes in different environmental factors. Here, we focused on the transmission of DNA methylation changes to naive male offspring after paternal exposure to either diet (~40\% less protein) or temperature increase (10 °C increased temperature). Because both experiments focused on the liver as the main metabolic and thermoregulation organ, we were able to decipher if epigenetic changes differed in response to different environmental changes. Reduced representation bisulfite sequencing (RRBS) revealed differentially methylated regions (DMRs) in annotated genomic regions in sons sired before (control) and after the fathers' treatments. We detected both a highly specific epigenetic response dependent on the environmental factor that had changed that was reflected in genes involved in specific metabolic pathways, and a more general response to changes in outer stimuli reflected by epigenetic modifications in a small subset of genes shared between both responses. Our results indicated that fathers prepared their offspring for specific environmental changes by paternally inherited epigenetic modifications, suggesting a strong paternal contribution to adaptive processes.}, language = {en} } @misc{LaemkeBaeurle2017, author = {L{\"a}mke, J{\"o}rn and B{\"a}urle, Isabel}, title = {Epigenetic and chromatin-based mechanisms in environmental stress adaptation and stress memory in plants}, series = {Postprints der Universit{\"a}t Potsdam Mathematisch-Naturwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam Mathematisch-Naturwissenschaftliche Reihe}, number = {792}, issn = {1866-8372}, doi = {10.25932/publishup-43623}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-436236}, pages = {11}, year = {2017}, abstract = {Plants frequently have to weather both biotic and abiotic stressors, and have evolved sophisticated adaptation and defense mechanisms. In recent years, chromatin modifications, nucleosome positioning, and DNA methylation have been recognized as important components in these adaptations. Given their potential epigenetic nature, such modifications may provide a mechanistic basis for a stress memory, enabling plants to respond more efficiently to recurring stress or even to prepare their offspring for potential future assaults. In this review, we discuss both the involvement of chromatin in stress responses and the current evidence on somatic, intergenerational, and transgenerational stress memory.}, language = {en} } @article{LaemkeBaeurle2017, author = {L{\"a}mke, J{\"o}rn and B{\"a}urle, Isabel}, title = {Epigenetic and chromatin-based mechanisms in environmental stress adaptation and stress memory in plants}, series = {Genome biology : biology for the post-genomic era}, volume = {18}, journal = {Genome biology : biology for the post-genomic era}, publisher = {BioMed Central}, address = {London}, issn = {1474-760X}, doi = {10.1186/s13059-017-1263-6}, pages = {8685 -- 8693}, year = {2017}, abstract = {Plants frequently have to weather both biotic and abiotic stressors, and have evolved sophisticated adaptation and defense mechanisms. In recent years, chromatin modifications, nucleosome positioning, and DNA methylation have been recognized as important components in these adaptations. Given their potential epigenetic nature, such modifications may provide a mechanistic basis for a stress memory, enabling plants to respond more efficiently to recurring stress or even to prepare their offspring for potential future assaults. In this review, we discuss both the involvement of chromatin in stress responses and the current evidence on somatic, intergenerational, and transgenerational stress memory.}, language = {en} } @article{SaussenthalerOuniBaumeieretal.2019, author = {Saussenthaler, Sophie and Ouni, Meriem and Baumeier, Christian and Schwerbel, Kristin and Gottmann, Pascal and Christmann, Sabrina and Laeger, Thomas and Sch{\"u}rmann, Annette}, title = {Epigenetic regulation of hepatic Dpp4 expression in response to dietary protein}, series = {The journal of nutritional biochemistry}, volume = {63}, journal = {The journal of nutritional biochemistry}, publisher = {Elsevier}, address = {New York}, issn = {0955-2863}, doi = {10.1016/j.jnutbio.2018.09.025}, pages = {109 -- 116}, year = {2019}, abstract = {Dipeptidyl peptidase 4 (DPP4) is known to be elevated in metabolic disturbances such as obesity, type 2 diabetes and fatty liver disease. Lowering DPP4 concentration by pharmacological inhibition improves glucose homeostasis and exhibits beneficial effects to reduce hepatic fat content. As factors regulating the endogenous expression of Dpp4 are unknown, the aim of this study was to examine whether the Dpp4 expression is epigenetically regulated in response to dietary components. Primary hepatocytes were treated with different macronutrients, and Dpp4 mRNA levels and DPP4 activity were evaluated. Moreover, dietary low-protein intervention was conducted in New Zealand obese (NZO) mice, and subsequently, effects on Dpp4 expression, methylation as well as plasma concentration and activity were determined. Our results indicate that Dpp4 mRNA expression is mediated by DNA methylation in several tissues. We therefore consider the Dpp4 southern shore as tissue differentially methylated region. Amino acids increased Dpp4 expression in primary hepatocytes, whereas glucose and fatty acids were without effect. Dietary protein restriction in NZO mice increased Dpp4 DNA methylation in liver leading to diminished Dpp4 expression and consequently to lowered plasma DPP4 activity. We conclude that protein restriction in the adolescent and adult states is a sufficient strategy to reduce DPP4 which in turn contributes to improve glucose homeostasis. (C) 2018 Published by Elsevier Inc.}, language = {en} } @article{GuerreroFickelBenhaiemetal.2020, author = {Guerrero, Tania P. and Fickel, J{\"o}rns and Benhaiem, Sarah and Weyrich, Alexandra}, title = {Epigenomics and gene regulation in mammalian social systems}, series = {Current zoology}, volume = {66}, journal = {Current zoology}, number = {3}, publisher = {Oxford Univ. Press}, address = {Oxford}, issn = {1674-5507}, doi = {10.1093/cz/zoaa005}, pages = {307 -- 319}, year = {2020}, abstract = {Social epigenomics is a new field of research that studies how the social environment shapes the epigenome and how in turn the epigenome modulates behavior. We focus on describing known gene-environment interactions (GEIs) and epigenetic mechanisms in different mammalian social systems. To illustrate how epigenetic mechanisms integrate GEls, we highlight examples where epigenetic mechanisms are associated with social behaviors and with their maintenance through neuroendocrine, locomotor, and metabolic responses. We discuss future research trajectories and open questions for the emerging field of social epigenomics in nonmodel and naturally occurring social systems. Finally, we outline the technological advances that aid the study of epigenetic mechanisms in the establishment of GEIs and vice versa.}, language = {en} } @article{KanzleiterJaehnertSchulzeetal.2015, author = {Kanzleiter, Timo and Jaehnert, Markus and Schulze, Gunnar and Selbig, Joachim and Hallahan, Nicole and Schwenk, Robert Wolfgang and Sch{\"u}rmann, Annette}, title = {Exercise training alters DNA methylation patterns in genes related to muscle growth and differentiation in mice}, series = {American journal of physiology : Endocrinology and metabolism}, volume = {308}, journal = {American journal of physiology : Endocrinology and metabolism}, number = {10}, publisher = {American Chemical Society}, address = {Bethesda}, issn = {0193-1849}, doi = {10.1152/ajpendo.00289.2014}, pages = {E912 -- E920}, year = {2015}, abstract = {The adaptive response of skeletal muscle to exercise training is tightly controlled and therefore requires transcriptional regulation. DNA methylation is an epigenetic mechanism known to modulate gene expression, but its contribution to exercise-induced adaptations in skeletal muscle is not well studied. Here, we describe a genome-wide analysis of DNA methylation in muscle of trained mice (n = 3). Compared with sedentary controls, 2,762 genes exhibited differentially methylated CpGs (P < 0.05, meth diff >5\%, coverage > 10) in their putative promoter regions. Alignment with gene expression data (n = 6) revealed 200 genes with a negative correlation between methylation and expression changes in response to exercise training. The majority of these genes were related to muscle growth and differentiation, and a minor fraction involved in metabolic regulation. Among the candidates were genes that regulate the expression of myogenic regulatory factors (Plexin A2) as well as genes that participate in muscle hypertrophy (Igfbp4) and motor neuron innervation (Dok7). Interestingly, a transcription factor binding site enrichment study discovered significantly enriched occurrence of CpG methylation in the binding sites of the myogenic regulatory factors MyoD and myogenin. These findings suggest that DNA methylation is involved in the regulation of muscle adaptation to regular exercise training.}, language = {en} }