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Epigenomes
Special Issues
Non-CpG Methylation
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Non-CpG Methylation

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

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 7324

Special Issue Editors

Dr. Marco Lucarelli

E-Mail Website
Guest Editor
1. Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy
2. Pasteur Institute Cenci Bolognetti Foundation, Sapienza University of Rome, Rome, Italy
Interests: cystic fibrosis; theratyping; epigenetics; gene expression; cellular differentiation; clinical molecular biology
Dr. Andrea Fuso

E-Mail Website
Guest Editor
Department of Experimental Medicine, Sapienza University of Rome, 00185 Roma, Italy
Interests: DNA methylation; epigenetics; nutrition; methylation metabolism; environmental epigenetics; neuroepigenetics; gene expression and chromatin biology; bisulfite sequencing; real-time PCR; Alzheimer’s disease; aging research; beta amyloid; neuroscience; neurobiology; neurodegenerative diseases; neurophysiology; neurodegeneration; neurobiology and brain physiology; animal models; cell culture; neurobiochemistry; methylation
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Special Issue Information

Dear Colleagues,

The DNA methylation, consisting in the presence of a methyl group (-CH3) on the carbon 5’ of the cytosine, represents the most known and most studied epigenetic mark, able to regulate the mRNA expression of the associated genes. Despite the very impressive bulk of studies related to DNA methylation mechanisms, dynamics, function and its physiological and even pathogenetic role, the scientific community has been stuck for years on the concept that >90% of DNA methylation in mammals occurs on the cytosines followed by a guanine, i.e. the CpG moieties. The possibility that DNA methylation at cytosines followed by other nucleotides, the so-called non-CpG methylation (or “CpN”, including CpA, CpT, CpC), remained confined to a small proportion of cytosines, considered non-functionally significant, except for embryonic tissues and stem cells. In the recent years, however, many evidences raised the possibility that the non-CpG methylation in adult and somatic tissues was underestimated due to technical biases and supported the idea that it could have functional role in driving gene expression.

The present Special Issue is aimed at collecting research articles and reviews that can draw the state-of-the-art on the role of non-CpG methylation in mammal cells, its dynamic regulation, structural patterning and role in pathogenic mechanisms.

Prof. Dr. Marco Lucarelli
Prof. Dr. Andrea Fuso
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.

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Published Papers (2 papers)

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Research

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13 pages, 2596 KiB  
Article
SNCA Gene Methylation in Parkinson’s Disease and Multiple System Atrophy
by Ekaterina Yu. Fedotova, Elena V. Iakovenko, Natalia Yu. Abramycheva and Sergey N. Illarioshkin
Epigenomes 2023, 7(1), 5; https://doi.org/10.3390/epigenomes7010005 - 6 Feb 2023
Cited by 5 | Viewed by 2908
Abstract
In recent years, epigenetic mechanisms have been implicated in the development of multifactorial diseases including neurodegenerative disorders. In Parkinson’s disease (PD), as a synucleinopathy, most studies focused on DNA methylation of SNCA gene coding alpha-synuclein but obtained results were rather contradictory. In another [...] Read more.
In recent years, epigenetic mechanisms have been implicated in the development of multifactorial diseases including neurodegenerative disorders. In Parkinson’s disease (PD), as a synucleinopathy, most studies focused on DNA methylation of SNCA gene coding alpha-synuclein but obtained results were rather contradictory. In another neurodegenerative synucleinopathy, multiple system atrophy (MSA), very few studies investigated the epigenetic regulation. This study included patients with PD (n = 82), patients with MSA (n = 24), and a control group (n = 50). In three groups, methylation levels of CpG and non-CpG sites in regulatory regions of the SNCA gene were analyzed. We revealed hypomethylation of CpG sites in the SNCA intron 1 in PD and hypermethylation of predominantly non-CpG sites in the SNCA promoter region in MSA. In PD patients, hypomethylation in the intron 1 was associated with earlier age at the disease onset. In MSA patients, hypermethylation in the promotor was associated with shorter disease duration (before examination). These results showed different patterns of the epigenetic regulation in two synucleinopathies—PD and MSA. Full article
(This article belongs to the Special Issue Non-CpG Methylation)
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Review

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9 pages, 1436 KiB  
Review
Experimental and Computational Approaches for Non-CpG Methylation Analysis
by Deepa Ramasamy, Arunagiri Kuha Deva Magendhra Rao, Thangarajan Rajkumar and Samson Mani
Epigenomes 2022, 6(3), 24; https://doi.org/10.3390/epigenomes6030024 - 16 Aug 2022
Cited by 2 | Viewed by 3412
Abstract
Cytosine methylation adjacent to adenine, thymine, and cytosine residues but not guanine of the DNA is distinctively known as non-CpG methylation. This CA/CT/CC methylation accounts for 15% of the total cytosine methylation and varies among different cell and tissue types. The abundance of [...] Read more.
Cytosine methylation adjacent to adenine, thymine, and cytosine residues but not guanine of the DNA is distinctively known as non-CpG methylation. This CA/CT/CC methylation accounts for 15% of the total cytosine methylation and varies among different cell and tissue types. The abundance of CpG methylation has largely concealed the role of non-CpG methylation. Limitations in the early detection methods could not distinguish CpG methylation from non-CpG methylation. Recent advancements in enrichment strategies and high throughput sequencing technologies have enabled the detection of non-CpG methylation. This review discusses the advanced experimental and computational approaches to detect and describe the genomic distribution and function of non-CpG methylation. We present different approaches such as enzyme-based and antibody-based enrichment, which, when coupled, can also improve the sensitivity and specificity of non-CpG detection. We also describe the current bioinformatics pipelines and their specific application in computing and visualizing the imbalance of CpG and non-CpG methylation. Enrichment modes and the computational suites need to be further developed to ease the challenges of understanding the functional role of non-CpG methylation. Full article
(This article belongs to the Special Issue Non-CpG Methylation)
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