Frontiers in epigenetics and epigenomics最新文献

{"title":"High-throughput, pan-leukocyte biomarkers for the detection of inflammation in human breastmilk and stool.","authors":"M J Dunnet, I M Morison, D M Bond, T A Hore","doi":"10.3389/freae.2025.1535838","DOIUrl":"10.3389/freae.2025.1535838","url":null,"abstract":"<p><strong>Background: </strong>DNA methylation can be used to track cellular identity. We have previously developed a high-throughput, cost-effective DNA methylation pipeline containing two loci, <i>HOXA3</i> and <i>MAP4K1</i>, that can quantify leukocyte proportion amongst a range of background tissues. Here, we apply this pipeline to two clinically relevant tissue samples: breastmilk and stool.</p><p><strong>Results: </strong>We report that our leukocyte methylation assay can quantify the proportion of leukocytes in breastmilk, and find leukocyte levels fluctuate dramatically in concert with infection severity. We benchmarked our leukocyte methylation pipeline in stool samples against the commonly used faecal calprotectin assay. Our results show a high concordance between the two methods indicating the viability of our DNA methylation biomarkers in the context of intestinal inflammation.</p><p><strong>Conclusion: </strong>The data presented here emphasise the clinical applicability of our high-throughput DNA methylation assay in the context of mastitis and intestinal inflammation.</p>","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"3 ","pages":"1535838"},"PeriodicalIF":0.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles for epigenetics in wood formation and stress response intrees-from basic biology to forest management.","authors":"Andrew Groover","doi":"10.3389/freae.2025.1476499","DOIUrl":"10.3389/freae.2025.1476499","url":null,"abstract":"<p><p>Annual model and crop species have been the subject of most epigenetic studies for plants. In contrast to annuals, forest trees persist on natural landscapes and experience environmental variation within and across seasons, years, and decades or even centuries. Most forest trees species are undomesticated and typically grown on variable landscapes with no irrigation or application of agricultural chemicals. Forest trees must thus rely on their inherent ability to alter growth and physiology to mitigate the effects of changing abiotic and biotic stressors. Like other plants, trees have mechanisms encoded in their genomic DNA sequence that can respond directly to stress events such as drought or heat. Hypothetically, it would be highly advantageous to join these mechanisms with a dynamic \"memory\" of past exposure to stress. It is now well established that annual model and crop plants can establish epigenetic-based memory of stress events that support more rapid and robust response to stress in the future. Here, evidence is discussed for epigenetic regulation and \"memory\" in two fundamental biological processes in trees, wood formation and abiotic stress response. Wood formation is an ideal trait for epigenetic research in trees, as wood formation is highly responsive to environmental conditions and includes multiple rapid developmental changes as cells adopt distinct fates within complex tissues. This is followed by a discussion of research needs that would provide the foundation for new epigenetic applications for forestry.</p>","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"3 ","pages":"1476499"},"PeriodicalIF":0.0,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13632498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Current insights in Epigenetics and Epigenomics.","authors":"Steven Henikoff, Sharon Y R Dent, Raul Mostoslavsky, Ting Wang, Luca Comai","doi":"10.3389/freae.2025.1566501","DOIUrl":"10.3389/freae.2025.1566501","url":null,"abstract":"","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"3 ","pages":"1566501"},"PeriodicalIF":0.0,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13632475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Epigenetics and genomic causality in development and chromatin research.","authors":"Ellen V Rothenberg, Ute Deichmann","doi":"10.3389/freae.2025.1564074","DOIUrl":"10.3389/freae.2025.1564074","url":null,"abstract":"","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"3 ","pages":"1564074"},"PeriodicalIF":0.0,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13632477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149122004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of entinostat, quisinostat, and tubastatin-A on alcohol consumption in male high ethanol consuming rats.","authors":"Sheketha R Hauser, Laura B Ferguson, Tiebing Liang, Erin E Jarvis, R Dayne Mayfield, Richard L Bell","doi":"10.3389/freae.2024.1503093","DOIUrl":"10.3389/freae.2024.1503093","url":null,"abstract":"<p><strong>Background: </strong>The interaction between genetics, epigenetics, and the environment plays a key role in the development of alcohol use disorder (AUD). Pharmacological treatments targeting histone deacetylases (HDACs) suggest that HDAC inhibitors (HDACi) may be potential pharmacotherapeutic treatments for AUD. The objective of the current study was to test the effects of different HDACi on ethanol intake in two rat lines selectively bred for high ethanol-consumption.</p><p><strong>Method: </strong>Adult naïve male high alcohol drinking line 1 (HAD1) or alcohol-preferring (P) rats were given continuous 24-h, 3-bottle, free-choice access to 15%, 30% ethanol concurrently with water for 8 weeks prior to testing entinostat (selective HDAC1i and HADC3i, 0, 1.25, 2.5, 5 mg/kg, i. p.), quisinostat (pan HADCi, 0, 0.5, 1.0, 2.0 mg/kg, i. p.), or tubastatin-A (selective HDAC6i, 0, 1.25, 2.5, 5 mg/kg, i. p.) over 4-5 consecutive days.</p><p><strong>Results: </strong>In HAD1 rats, entinostat reduced 2-, 4-, and 24-h ethanol intake across the 2^nd - 5^th test days; while, in P rats, entinostat's effect was primarily seen at the 24-h time-point, at the highest dose and only across three test days. The high dose of quisinostat effectively reduced 24-h ethanol intake across the 1^st-4^th test days in HAD1 rats but was ineffective in P rats. Tubastatin-A did not alter ethanol intake in either rat line.</p><p><strong>Conclusion: </strong>Overall, the results confirmed that a pan and a more selective (HDAC1 and HDAC3) HDACi effectively reduced ethanol intake in HAD1, while only the more selective HDACi reduced ethanol intake in P rats. Inhibition of HDAC6 does not appear to regulate ethanol intake in HAD1 or P rats.</p>","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"2 ","pages":"1503093"},"PeriodicalIF":0.0,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13632490/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lineage- and stage-specific activity of antigen receptor gene enhancers during lymphocyte development.","authors":"Fei Ma, Fatima Zohra Braikia, Ranjan Sen","doi":"10.3389/freae.2024.1489362","DOIUrl":"10.3389/freae.2024.1489362","url":null,"abstract":"<p><p>Lymphocyte development culminates with generation of mature B and T cells that express unique antigen receptors on the cell surface. Genes that encode the two chains of B or T cell receptors are generated via DNA recombination and expressed sequentially during development, guided by locus activating enhancer sequences. In this review we summarize our understanding of molecular mechanisms that activate these enhancers in a lineage and developmental stage-specific manner. We draw attention to 1) the distinction between chromatin accessibility and transcriptional activation of these loci, 2) incomplete understanding of mechanisms that regulate B versus T cell-specific enhancer activity and 3) transcription factors that contribute to stage-specific enhancer activation within each lineage.</p>","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"2 ","pages":"1489362"},"PeriodicalIF":0.0,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of climate change-related disasters on mental health and epigenetics: a narrative review.","authors":"Emma Antonina Roe, Engluy Khov, Hannah Kim, Beth Demelo, Savannah Zavitz, Lei Cao-Lei","doi":"10.3389/freae.2024.1464276","DOIUrl":"10.3389/freae.2024.1464276","url":null,"abstract":"<p><p>Climate change has contributed to an increase in the frequency and intensity of natural disasters such as droughts, wildfires, hurricanes, and floods, leading to both immediate physical harm and long-term mental health consequences. Survivors often experience psychological distress, including anxiety, depression, and post-traumatic stress disorder (PTSD), as a result of these traumatic events. This narrative review explores the intersection of climate change-related disasters, mental health outcomes, and epigenetic modifications. Specifically, we summarize recent findings on how environmental stressors influence both mental health and epigenetic changes, such as DNA methylation. Emerging evidence suggests that epigenetic mechanisms, particularly DNA methylation, could mediate the effects of climate change-related stress on mental health, potentially contributing to the onset of mental disorders like depression, panic disorder, autism spectrum disorder, and attention deficit hyperactivity disorder. We also discuss other epigenetic mechanisms, such as histone modifications and non-coding RNAs, and emphasize the importance of longitudinal studies to capture the dynamic nature of epigenetic changes over time. Finally, we propose future research directions to deepen our understanding of the complex relationships between climate change-related disasters, mental health outcomes, and epigenetic mechanisms, which will pave the way for more effective mental health interventions and policy integration.</p>","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"2 ","pages":"1464276"},"PeriodicalIF":0.0,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13632494/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blood DNA methylation of <i>CRF</i> and its association with amygdala volume and mood in Cushing's syndrome.","authors":"Richard S Lee, Alicia Santos, Henri Garrison-Desany, Anna Aulinas, Jenny L Carey, Yolanda Vives-Gilabert, Olivia H Cox, Gabriel Cuilan, Susan M Webb, Eugenia Resmini","doi":"10.3389/freae.2024.1435634","DOIUrl":"10.3389/freae.2024.1435634","url":null,"abstract":"<p><strong>Objective: </strong>The impact of chronic exposure to stress or glucocorticoids on psychiatric symptoms has been exemplified by cases of iatrogenic or endogenous hypercortisolism such as Cushing's syndrome (CS). The amygdala plays an important role in mediating both stress and affective responses, and one of the key factors that link stress response and psychiatric symptoms is the corticotropin-releasing factor (CRF). Epigenetic changes, especially those occurring on CpG dinucleotides in DNA of glucocorticoid target genes in blood, have been previously implicated as potential predictors of glucocorticoid-related events in the central nervous system (CNS). In this study, we examined amygdala volume and mood symptoms in CS patients and aimed at evaluating whether these parameters were associated with blood DNA methylation of <i>CRF</i>.</p><p><strong>Methods: </strong>In this cross-sectional study, 32 CS patients and 32 healthy controls matched for age, sex, and years of education underwent an MRI scan, a Beck Depression Inventory-II, and a State-Trait Anxiety Inventory. Genomic DNA extracted from total leukocytes were used for DNA methylation analysis of several CpG dinucleotides at the <i>CRF</i> promoter region.</p><p><strong>Results: </strong>Significant associations between <i>CRF</i> methylation vs. amygdala volume (CpG-1, <i>P</i> = 0.006) and depression scores (CpG-2, <i>P</i> = 0.01) were found. To assess whether the promoter CpG methylation has functional consequences, we examined RNA and DNA extracted from non-CS, postmortem amygdala tissues. A significant association between CpG methylation and gene expression (CpG-1, <i>P</i> = 0.004) was observed.</p><p><strong>Conclusion: </strong>These results demonstrate that methylation levels of the <i>CRF</i> promoter CpGs are associated with amygdala volume in CS and related mood symptoms. Methylation levels may also be associated with <i>CRF</i> expression. This finding supports the feasibility of using epigenetic patterns in blood as a surrogate for assessing GC-related pathologies in the brain.</p>","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"2 ","pages":"1435634"},"PeriodicalIF":0.0,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of developmentally controlled enhancer activity by extrinsic signals in normal and malignant cells: AP-1 at the centre.","authors":"Alexander Maytum, Nadine Obier, Pierre Cauchy, Constanze Bonifer","doi":"10.3389/freae.2024.1465958","DOIUrl":"10.3389/freae.2024.1465958","url":null,"abstract":"<p><p>The ability of cells to respond to external stimuli is one of the characteristics of life as we know it. Multicellular organisms have developed a huge machinery that interprets the cellular environment and instigates an appropriate cellular response by changing gene expression, metabolism, proliferation state and motility. Decades of research have studied the pathways transmitting the various signals within the cell. However, whilst we know most of the players, we know surprisingly little about the mechanistic details of how extrinsic signals are interpreted and integrated within the genome. In this article we revisit the long-standing debate of whether factors regulating cellular growth (cytokines) act in an instructive or permissive fashion on cell fate decisions. We touch upon this topic by highlighting the paradigm of AP-1 as one of the most important signaling-responsive transcription factor family and summarize our work and that of others to explain what is known about cytokine responsive cis-regulatory elements driving differential gene expression. We propose that cytokines and, by extension, multiple types of external signals are the main drivers of cell differentiation and act via inducible transcription factors that transmit signaling processes to the genome and are essential for changing gene expression to drive transitions between gene regulatory networks. Importantly, inducible transcription factors cooperate with cell type specific factors within a pre-existing chromatin landscape and integrate multiple signaling pathways at specific enhancer elements, to both maintain and alter cellular identities. We also propose that signaling processes and signaling responsive transcription factors are at the heart of tumor development.</p>","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"2 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7616781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142592451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay between epigenetics and metabolism controls cancer stem cell plasticity.","authors":"Jee-Eun Choi, Inwha Baek","doi":"10.3389/freae.2024.1424163","DOIUrl":"10.3389/freae.2024.1424163","url":null,"abstract":"<p><p>Tumors consist of cancer cells with different genetic, epigenetic, and phenotypic properties. Cancer stem cells are an important subpopulation of heterogeneous cancer cells and are capable of initiating and propagating tumors. The term cancer stem cells has become broader in efforts to understand their phenotypic plasticity to switch fates between self-renewal and differentiation. Cancer stem cell plasticity is significantly associated with the initiation of metastasis, resistance to therapy, and tumor recurrence. With our broadened knowledge of epigenetic regulation and metabolic reprogramming as key elements enabling such capabilities, an expansive body of literature has demonstrated the functional importance of each element in contributing to cancer stem cell characteristics. Recently, the direct interplay between epigenetic regulation and metabolic reprogramming has begun to be appreciated in the context of cancer stem cells with growing interest. In this review, we discuss the mechanisms by which cancer stem cells orchestrate the reciprocal regulation of cellular metabolism and epigenetic alterations. In the discussion, compelling, unanswered questions on this topic have been elaborated for the interest of the research community and how recent technological developments help tackle such research ideas. A comprehensive understanding of cancer stem cell attributes that are largely governed by epigenetic and metabolic reprogramming would enable the advancement of precise therapeutic options and the prediction of better responses to drugs, holding great promise in cancer treatment and cure.</p>","PeriodicalId":101353,"journal":{"name":"Frontiers in epigenetics and epigenomics","volume":"2 ","pages":"1424163"},"PeriodicalIF":0.0,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639278/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149121610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}