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Epigenomes
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Epigenetics of the Nervous System
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Epigenetics of the Nervous System

A special issue of Epigenomes (ISSN 2075-4655).

Deadline for manuscript submissions: closed (15 July 2018) | Viewed by 34229

Special Issue Editors

Prof. Dr. Che-Kun James Shen

E-Mail Website
Guest Editor
1. The PhD Program for Neural Regenerative Medicine, Taipei Medical University, Taipei 115, Taiwan
2. Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan
Interests: gene regulation; chromatin; DNA methylation; neurofunction; transcription
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Guoping Fan

E-Mail Website
Guest Editor
Department of Human Genetics, David Geffen School of Medicine, University of California Los Angeles, Gonda BLDG Rm. 6554, P.O. Box 957088, Los Angeles, CA 90095-7088, USA
Interests: epigenetics; gene expression; DNA methylation; neural stem cell differentiation; adult brain function; somatic cell reprogramming
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The Open Access journal Epigenomes is now accepting submissions for this special issue on biological methylation, “Epigenetics of the Nervous System”. This special issue is co-guest-edited by Dr. Guoping Fan from the Department of Human Genetics, University of California, Los Angeles, and Dr. Che-Kun James Shen from the Institute of Molecular Biology, Academia Sinica, in Taiwan. This Special Issue will include commissioned topical reviews written by leaders in the field. Accepted papers are published online shortly after copy editing. There are no Article Processing Charges (APCs) for papers submitted in 2016.

In the last few years, epigenetic modifications in the nervous system have proven to be fundamental for the correct development and function of the brain. It is well known that DNA methylation is associated with learning as well as with the development of several neurological disorders including neurodegeneration.

This special issue will be focused on epigenetic changes that take place in the nervous system, from adolescent development through adulthood. In addition to invited reviews, we welcome Research and/or Methods manuscripts of exceptional interest on the following topics:

Effect of epigenetic changes in neural stem cells
Epigenetics and neuropathology
Animal models for the study of the relationship between epigenetics and the nervous system
Human neural pathologies and epigenetics

Dr. Guoping Fan
Dr. Che-Kun James Shen
Guest Editors

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. Epigenomes is an international peer-reviewed open access quarterly 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 1500 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
  • Neural plasticity
  • Neural pathology
  • Stem cells
  • Cell differentiation
  • Epigenetics and Neuronal Activities

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Published Papers (5 papers)

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Editorial

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4 pages, 176 KiB  
Editorial
Non-CpG Methylation Revised
by Andrea Fuso
Epigenomes 2018, 2(4), 22; https://doi.org/10.3390/epigenomes2040022 - 12 Dec 2018
Cited by 8 | Viewed by 4580
Abstract
Textbook and scientific papers addressing DNA methylation usually still cite “DNA methylation occurs at CpG cytosines”. Methylation at cytosines outside the CpG nucleotide, the so-called “non-CpG methylation”, is usually considered a minor and not biologically relevant process. However, the technical improvements and additional [...] Read more.
Textbook and scientific papers addressing DNA methylation usually still cite “DNA methylation occurs at CpG cytosines”. Methylation at cytosines outside the CpG nucleotide, the so-called “non-CpG methylation”, is usually considered a minor and not biologically relevant process. However, the technical improvements and additional studies in epigenetics have demonstrated that non-CpG methylation is present with frequency higher than previously thought and retains biological activity, potentially relevant to the understanding and the treatment of human diseases. Full article
(This article belongs to the Special Issue Epigenetics of the Nervous System)

Review

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1394 KiB  
Review
Molecular and Epigenetic Mechanisms Underlying Cognitive and Adaptive Responses to Stress
by Alexandra F. Trollope, Karen R. Mifsud, Emily A. Saunderson and Johannes M. H. M. Reul
Epigenomes 2017, 1(3), 17; https://doi.org/10.3390/epigenomes1030017 - 2 Nov 2017
Cited by 6 | Viewed by 8005
Abstract
Consolidation of contextual memories after a stressful encounter is essential for the survival of an organism and in allowing a more appropriate response to be elicited should the perceived threat reoccur. Recent evidence has explored the complex role that epigenetic mechanisms play in [...] Read more.
Consolidation of contextual memories after a stressful encounter is essential for the survival of an organism and in allowing a more appropriate response to be elicited should the perceived threat reoccur. Recent evidence has explored the complex role that epigenetic mechanisms play in the formation of such memories, and the underlying signaling pathways are becoming more apparent. The glucocorticoid receptor (GR) has been shown to play a key role in these events having both genomic and non-genomic actions in the brain. GR has been shown to interact with the extracellular signal-regulated kinase mitogen-activated protein kinase (ERK MAPK) signaling pathway which, in concert, drives epigenetic modifications and chromatin remodeling, resulting in gene induction and memory consolidation. Evidence indicates that stressful events can have an effect on the offspring in utero, and that epigenetic marks altered early in life may persist into adulthood. A new and controversial area of research, however, suggests that epigenetic modifications could be inherited through the germline, a concept known as transgenerational epigenetics. This review explores the role that epigenetic processes play in the central nervous system, specifically in the consolidation of stress-induced memories, the concept of transgenerational epigenetic inheritance, and the potential role of epigenetics in revolutionizing the treatment of stress-related disorders through the emerging field of pharmacoepigenetics and personalized medical treatment. Full article
(This article belongs to the Special Issue Epigenetics of the Nervous System)
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468 KiB  
Review
EHMT1/GLP; Biochemical Function and Association with Brain Disorders
by Manal A. Adam and Anthony R. Isles
Epigenomes 2017, 1(3), 15; https://doi.org/10.3390/epigenomes1030015 - 19 Oct 2017
Cited by 5 | Viewed by 7432
Abstract
The gene EHMT1 that encodes the Euchromatic Histone Methyltransferase-1, also known as GLP (G9a-like protein), has been associated with a number of neurodevelopmental and neurodegenerative disorders. GLP is a member of the euchromatic lysine histone methyltransferase family, along with EHMT2 or G9A. As [...] Read more.
The gene EHMT1 that encodes the Euchromatic Histone Methyltransferase-1, also known as GLP (G9a-like protein), has been associated with a number of neurodevelopmental and neurodegenerative disorders. GLP is a member of the euchromatic lysine histone methyltransferase family, along with EHMT2 or G9A. As its name implies, Ehmt1/GLP is involved in the addition of methyl groups to histone H3 lysine 9, a generally repressive mark linked to classical epigenetic process such as genomic imprinting, X-inactivation, and heterochromatin formation. However, GLP also plays both a direct and indirect role in regulating DNA-methylation. Here, we discuss what is currently known about the biochemical function of Ehmt1/GLP and its association, via various genetic studies, with brain disorders. Full article
(This article belongs to the Special Issue Epigenetics of the Nervous System)
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Figure 1

961 KiB  
Review
Epitranscriptome and FMRP Regulated mRNA Translation
by Pritha Majumder, Biswanath Chatterjee and C.-K. James Shen
Epigenomes 2017, 1(2), 11; https://doi.org/10.3390/epigenomes1020011 - 21 Jul 2017
Cited by 2 | Viewed by 6952
Abstract
An important regulatory mechanism affecting mRNA translation involves various covalent modifications of RNA, which establish distinct epitranscriptomic signatures that actively influence various physiological processes. Dendritic translation in mammalian neurons is a potent target for RNA modification-based regulation. In this mini-review, we focus on [...] Read more.
An important regulatory mechanism affecting mRNA translation involves various covalent modifications of RNA, which establish distinct epitranscriptomic signatures that actively influence various physiological processes. Dendritic translation in mammalian neurons is a potent target for RNA modification-based regulation. In this mini-review, we focus on the effect of potential RNA modifications on the spatiotemporal regulation of the dendritic translation of mRNAs, which are targeted by two important neuronal translational co-regulators, namely TDP-43 and Fragile X Mental Retardation Protein (FMRP). Full article
(This article belongs to the Special Issue Epigenetics of the Nervous System)
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1068 KiB  
Review
Driver or Passenger: Epigenomes in Alzheimer’s Disease
by Anke Hoffmann, Vincenza Sportelli, Michael Ziller and Dietmar Spengler
Epigenomes 2017, 1(1), 5; https://doi.org/10.3390/epigenomes1010005 - 30 Apr 2017
Cited by 2 | Viewed by 6310
Abstract
Alzheimer’s disease (AD) is a fatal neurodegenerative disease which is on the rise worldwide. Despite a wealth of information, genetic factors contributing to the emergence of AD still remain incompletely understood. Sporadic AD is polygenetic in nature and is associated with various environmental [...] Read more.
Alzheimer’s disease (AD) is a fatal neurodegenerative disease which is on the rise worldwide. Despite a wealth of information, genetic factors contributing to the emergence of AD still remain incompletely understood. Sporadic AD is polygenetic in nature and is associated with various environmental risks. Epigenetic mechanisms are well-recognized in the mediation of gene environment interactions, and analysis of epigenetic changes at the genome scale can offer new insights into the relationship between brain epigenomes and AD. In fact, recent epigenome-wide association studies (EWAS) indicate that changes in DNA methylation are an early event preceding clinical manifestation and are tightly associated with AD neuropathology. Further, candidate genes from EWAS interact with those from genome-wide association studies (GWAS) that can undergo epigenetic changes in their upstream gene regulatory elements. Functionally, AD-associated DNA methylation changes partially influence transcription of candidate genes involved in pathways relevant to AD. The timing of epigenomic changes in AD together with the genes affected indicate a critical role, however, further mechanistic insight is required to corroborate this hypothesis. In this respect, recent advances in neuronal reprogramming of patient-derived cells combined with new genome-editing techniques offer unprecedented opportunities to dissect the functional and mechanistic role of epigenomic changes in AD. Full article
(This article belongs to the Special Issue Epigenetics of the Nervous System)
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