L. V. Yushko, A. D. Shevlyakov, M. A. Romazeva, K. V. Apukhtin, A. D. Volgin, D. A. Abramov, M. M. Kotova, A. V. Kalueff
{"title":"The Role of DNA Methylation in Zebrafish Models of CNS Diseases","authors":"L. V. Yushko, A. D. Shevlyakov, M. A. Romazeva, K. V. Apukhtin, A. D. Volgin, D. A. Abramov, M. M. Kotova, A. V. Kalueff","doi":"10.1134/s0022093024030104","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>DNA methylation plays an important role in the regulation\nof gene expression. Its deficits in the brain cause various neurological\ndiseases, including autism, schizophrenia and mood disorders. The\nzebrafish (<i>Danio rerio</i>) is\na promising model organism in biomedicine. Given its high genetic\nand physiological homology with humans, studying genome methylation\ndeficits in zebrafish can help elucidate the molecular processes\nunderlying the etiology and pathogenesis of various neurological\ndiseases, as well as develop novel therapies. Here, we discuss the\nmechanisms of DNA methylation in the brain and the diseases associated\nwith its dysregulation in humans, as well as their genetic and pharmacological\nmodels in zebrafish. We also evaluate the limitations of zebrafish\nmodels and possible directions for further research in this field.\nMounting evidence summarized here supports zebrafish as an effective\nmodel for elucidating the molecular mechanisms of brain pathologies\nassociated with compromised DNA methylation.</p>","PeriodicalId":15805,"journal":{"name":"Journal of Evolutionary Biochemistry and Physiology","volume":"75 1","pages":""},"PeriodicalIF":0.5000,"publicationDate":"2024-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Evolutionary Biochemistry and Physiology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1134/s0022093024030104","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
DNA methylation plays an important role in the regulation
of gene expression. Its deficits in the brain cause various neurological
diseases, including autism, schizophrenia and mood disorders. The
zebrafish (Danio rerio) is
a promising model organism in biomedicine. Given its high genetic
and physiological homology with humans, studying genome methylation
deficits in zebrafish can help elucidate the molecular processes
underlying the etiology and pathogenesis of various neurological
diseases, as well as develop novel therapies. Here, we discuss the
mechanisms of DNA methylation in the brain and the diseases associated
with its dysregulation in humans, as well as their genetic and pharmacological
models in zebrafish. We also evaluate the limitations of zebrafish
models and possible directions for further research in this field.
Mounting evidence summarized here supports zebrafish as an effective
model for elucidating the molecular mechanisms of brain pathologies
associated with compromised DNA methylation.
摘要 DNA 甲基化在调控基因表达方面发挥着重要作用。它在大脑中的缺陷会导致各种神经疾病，包括自闭症、精神分裂症和情绪障碍。斑马鱼（Danio rerio）是一种很有前途的生物医学模式生物。鉴于斑马鱼与人类在遗传和生理方面的高度同源性，研究斑马鱼基因组甲基化缺陷有助于阐明各种神经疾病的病因和发病机制的分子过程，并开发新型疗法。在这里，我们讨论了大脑中 DNA 甲基化的主题机制和人类中与甲基化失调相关的疾病，以及它们在斑马鱼中的遗传和药理学模型。本文总结的大量证据表明，斑马鱼是阐明与 DNA 甲基化受损相关的大脑病理分子机制的有效模型。
期刊介绍：
Journal of Evolutionary Biochemistry and Physiology publishes original experimental and theoretical and review articles related to evolution of the main forms of metabolism in connection with life origin; comparative and ontogenetic physiology and biochemistry, biochemical evolution of animal world; as well as evolution of functions; morphology, pharmacology, pathophysiology and ecological physiology. The journal welcomes manuscripts from all countries in the English or Russian language.
京公网安备 11010802042870号
京ICP备2023020795号-1
分享
求助内容：
应助结果提醒方式：
扫码关注我们
