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Cells
Special Issues
Epigenetic Control and Gene Regulatory Mechanisms in Development and Disease
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Epigenetic Control and Gene Regulatory Mechanisms in Development and Disease

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 2005

Special Issue Editor

Prof. Dr. Mojgan Rastegar

E-Mail Website
Guest Editor
Department of Biochemistry and Medical Genetics, Rady Faculty of Health Sciences, Max Rady College of Medicine, University of Manitoba, Winnipeg, MB R3E 0J9, Canada
Interests: epigenetics; DNA methylation; transcriptional control; gene regulation; drug repurposing; neural stem cells; neurodevelopmental disorders; medulloblastoma brain tumor
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epigenetics refer to a wide range of regulatory mechanisms that control gene expression to determine cellular morphology and function. Such mechanisms include multi-step regulation at the level of gene transcription, post-transcription, protein translation, and post-translational control. The route to embryonic and postnatal development, and stem cell differentiation are complex and well-programmed processes that are tightly regulated at both genetic and epigenetic levels. Genetic mutations or epigenetic deregulation, in part influenced by environmental factors, may lead to impaired development and in many cases cause human diseases.

This Special Issue aims to provide an up to date platform for original research and review papers that cover subjects related to different forms of epigenetic mechanisms, including DNA, RNA, and histone modifications, regulatory RNA molecules, alternative splicing and related factors, three-dimensional chromatin structure, enhancer–promoter interactions, nucleosome remodeling, as well as the role of epigenetic factors (readers, writers, and erasers). Epigenetic mechanisms are important in development and disease and relevant subjects are welcome for submission, along with studies related to associated model systems.

Prof. Dr. Mojgan Rastegar
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • epigenetics
  • gene regulation
  • mammalian development
  • human disease
  • stem cells

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Published Papers (1 paper)

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Research

24 pages, 2343 KiB  
Article
Altered Epigenetic Marks and Gene Expression in Fetal Brain, and Postnatal Behavioural Disorders, Following Prenatal Exposure of Ogg1 Knockout Mice to Saline or Ethanol
by Shama Bhatia, David Bodenstein, Ashley P. Cheng and Peter G. Wells
Cells 2023, 12(18), 2308; https://doi.org/10.3390/cells12182308 - 19 Sep 2023
Cited by 1 | Viewed by 1603
Abstract
Oxoguanine glycosylase 1 (OGG1) is widely known to repair the reactive oxygen species (ROS)-initiated DNA lesion 8-oxoguanine (8-oxoG), and more recently was shown to act as an epigenetic modifier. We have previously shown that saline-exposed Ogg1 −/− knockout progeny exhibited learning and memory [...] Read more.
Oxoguanine glycosylase 1 (OGG1) is widely known to repair the reactive oxygen species (ROS)-initiated DNA lesion 8-oxoguanine (8-oxoG), and more recently was shown to act as an epigenetic modifier. We have previously shown that saline-exposed Ogg1 −/− knockout progeny exhibited learning and memory deficits, which were enhanced by in utero exposure to a single low dose of ethanol (EtOH) in both Ogg1 +/+ and −/− progeny, but more so in Ogg1 −/− progeny. Herein, OGG1-deficient progeny exposed in utero to a single low dose of EtOH or its saline vehicle exhibited OGG1- and/or EtOH-dependent alterations in global histone methylation and acetylation, DNA methylation and gene expression (Tet1 (Tet Methylcytosine Dioxygenase 1), Nlgn3 (Neuroligin 3), Hdac2 (Histone Deacetylase 2), Reln (Reelin) and Esr1 (Estrogen Receptor 1)) in fetal brains, and behavioural changes in open field activity, social interaction and ultrasonic vocalization, but not prepulse inhibition. OGG1- and EtOH-dependent changes in Esr1 and Esr2 mRNA and protein levels were sex-dependent, as was the association of Esr1 gene expression with gene activation mark histone H3 lysine 4 trimethylation (H3K4me3) and gene repression mark histone H3 lysine 27 trimethylation (H3K27me3) measured via ChIP-qPCR. The OGG1-dependent changes in global epigenetic marks and gene/protein expression in fetal brains, and postnatal behavioural changes, observed in both saline- and EtOH-exposed progeny, suggest the involvement of epigenetic mechanisms in developmental disorders mediated by 8-oxoG and/or OGG1. Epigenetic effects of OGG1 may be involved in ESR1-mediated gene regulation, which may be altered by physiological and EtOH-enhanced levels of ROS formation, possibly contributing to sex-dependent developmental disorders observed in Ogg1 knockout mice. The OGG1- and EtOH-dependent associations provide a basis for more comprehensive mechanistic studies to determine the causal involvement of oxidative DNA damage and epigenetic changes in ROS-mediated neurodevelopmental disorders. Full article
(This article belongs to the Special Issue Epigenetic Control and Gene Regulatory Mechanisms in Development and Disease)
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