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Biology
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Epigenetic Mechanisms Underlying Brain Development and Neuronal Activity
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Epigenetic Mechanisms Underlying Brain Development and Neuronal Activity

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Genetics and Genomics".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 10755

Special Issue Editors

Prof. Dr. Hehuang Xie

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Guest Editor
Department of Biomedical Sciences and Pathobiology, Virginia-Maryland College of Veterinary Medicine, Blacksburg, VA 24061, USA
Interests: brain development; epigenetics; epitranscriptomics; transcriptional regulation; computational biology; bioinformatics
Dr. Anna R. Moore

E-Mail Website
Guest Editor
Department of Biology, Temple University, 1900 N 12th St, Philadelphia, PA 19122, USA
Interests: circuit function; cortical development; plasticity; activity-dependent gene regulation; electrophysiology
Prof. Dr. Wucheng Tao

E-Mail Website
Guest Editor
Key Laboratory of Brain Aging and Neurodegenerative Diseases, Fujian Medical University, Fuzhou, China
Interests: synaptic transmission; synaptic plasticity; hippocampal circuit; memory; electrophysiology

Special Issue Information

Dear Colleagues,

Brain development is a highly orchestrated series of events relying on a tight interplay between innate genetic programs and neural activity to shape the formation of neural circuits. This tight interplay between activity and gene regulation is present at all stages of development, including cell proliferation, migration, differentiation and circuit formation and refinement. During early brain development, neural progenitor cells gain ample diversity at the level of epigenomics and differentiate into a population of heterogeneous cells. In fact, the epigenomic programming of brain cells involves numerous molecular and cellular processes to direct the changes in DNA methylation, histone and RNA modifications. As neural cell types are specified and differentiated, epigenetic mechanisms continue to shape brain function by serving as a key interface between environment stimuli and long lasting molecular, cellular and complex behavioral phenotypes. 

This research topic welcomes manuscripts presenting exciting advances in the field of epigenetics/epi-transcriptomics in brain tissue development, cellular function specification, aging, and neurodevelopmental disorders. Topics of interest include, but are not limited to, the following sections:

I. Mechanisms in the regulation of brain function and behavior with regard to histone modifications and DNA methylation.

II. Mechanisms in the regulation of brain functional roles via RNA methylation including N6-methyladenosine (m6A), 5-methylcytosine (5mC), and 5-hydroxymethylcytosine (5hmC).

III. Crosstalk among transcription factors and the machinery of histone and DNA modifications during brain development at all developmental stages: cell proliferation, migration, differentiation, and circuit formation and refinement.

IV. Large-scale genetic or epigenetic marker discovery linked to neurodevelopmental disorders.

V. Bioinformatics tools with novel statistical approaches, machine learning, neural nets or computational procedures/pipelines to provide unique insight in data interpretation for brain single cell analysis, “omics” data integration and mining.

VI. Review articles on the latest advances in brain epigenetic mechanisms or recent development of experimental and analytical tools for (DNA/RNA)-epigenetic/omics studies with applications to neural/brain disorders and aging progression. 

Prof. Dr. Hehuang Xie
Dr. Anna R. Moore
Prof. Dr. Wucheng Tao
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. Biology is an international peer-reviewed open access monthly 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.

Published Papers (4 papers)

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Research

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11 pages, 1113 KiB  
Article
Epigenetic Clock Explains White Matter Hyperintensity Burden Irrespective of Chronological Age
by Joan Jiménez-Balado, Eva Giralt-Steinhauer, Isabel Fernández-Pérez, Lucía Rey, Elisa Cuadrado-Godia, Ángel Ois, Ana Rodríguez-Campello, Carolina Soriano-Tárraga, Uxue Lazcano, Adrià Macias-Gómez, Antoni Suárez-Pérez, Anna Revert, Isabel Estragués, Brigitte Beltrán-Mármol, Santiago Medrano-Martorell, Jaume Capellades, Jaume Roquer and Jordi Jiménez-Conde
Biology 2023, 12(1), 33; https://0-doi-org.brum.beds.ac.uk/10.3390/biology12010033 - 24 Dec 2022
Cited by 4 | Viewed by 3102
Abstract
In this manuscript we studied the relationship between WMH and biological age (B-age) in patients with acute stroke. We included in this study 247 patients with acute stroke recruited at Hospital del Mar having both epigenetic (DNA methylation) and magnetic resonance imaging data. [...] Read more.
In this manuscript we studied the relationship between WMH and biological age (B-age) in patients with acute stroke. We included in this study 247 patients with acute stroke recruited at Hospital del Mar having both epigenetic (DNA methylation) and magnetic resonance imaging data. WMH were measured using a semi-automated method. B-age was calculated using two widely used methods: the Hannum and Horvath formulas. We used multiple linear regression models to interrogate the role of B-age on WMH volume after adjusting for chronological age (C-age) and other covariables. Average C-age of the sample was 68.4 (±11.8) and we observed a relatively high median WMH volume (median = 8.8 cm3, Q1–Q3 = 4.05–18.8). After adjusting for potential confounders, we observed a significant effect of B-ageHannum on WMH volume (βHannum = 0.023, p-value = 0.029) independently of C-age, which remained significant (βC-age = 0.021, p-value = 0.036). Finally, we performed a mediation analysis, which allowed us to discover that 42.7% of the effect of C-age on WMH is mediated by B-ageHannum. On the other hand, B-ageHoarvath showed no significant associations with WMH after being adjusted for C-age. In conclusion, we show for the first time that biological age, measured through DNA methylation, contributes substantially to explain WMH volumetric burden irrespective of chronological age. Full article
(This article belongs to the Special Issue Epigenetic Mechanisms Underlying Brain Development and Neuronal Activity)
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19 pages, 7307 KiB  
Article
Neuronal Depolarization Induced RNA m5C Methylation Changes in Mouse Cortical Neurons
by Xiguang Xu, Zachary Johnson and Hehuang Xie
Biology 2022, 11(7), 988; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11070988 - 29 Jun 2022
Cited by 1 | Viewed by 2011
Abstract
Neuronal activity is accomplished via substantial changes in gene expression, which may be accompanied by post-transcriptional modifications including RNA cytosine-5 methylation (m5C). Despite several reports on the transcriptome profiling of activated neurons, the dynamics of neuronal mRNA m5C modification [...] Read more.
Neuronal activity is accomplished via substantial changes in gene expression, which may be accompanied by post-transcriptional modifications including RNA cytosine-5 methylation (m5C). Despite several reports on the transcriptome profiling of activated neurons, the dynamics of neuronal mRNA m5C modification in response to environmental stimuli has not been explored. Here, we provide transcriptome-wide maps of m5C modification, together with gene expression profiles, for mouse cortical neurons at 0 h, 2 h, and 6 h upon membrane depolarization. Thousands of differentially expressed genes (DEGs) were identified during the neuronal depolarization process. In stimulated neurons, the majority of early response genes were found to serve as expression regulators of late response genes, which are involved in signaling pathways and diverse synaptic functions. With RNA bisulfite sequencing data, a union set of 439 m5C sites was identified with high confidence, and approximately 30% of them were shared by neurons at all three time points. Interestingly, over 41% of the m5C sites showed increased methylation upon neuronal activation and were enriched in transcripts coding for proteins with synaptic functions. In addition, a modest negative correlation was observed between RNA expression and methylation. In summary, our study provided dynamic transcriptome-wide landscapes of RNA m5C methylation in neurons, and revealed that mRNA m5C methylation is associated with the regulation of gene expression. Full article
(This article belongs to the Special Issue Epigenetic Mechanisms Underlying Brain Development and Neuronal Activity)
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Review

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35 pages, 1080 KiB  
Review
Intergenerational Perioperative Neurocognitive Disorder
by Ling-Sha Ju, Timothy E. Morey, Christoph N. Seubert and Anatoly E. Martynyuk
Biology 2023, 12(4), 567; https://0-doi-org.brum.beds.ac.uk/10.3390/biology12040567 - 7 Apr 2023
Cited by 3 | Viewed by 1694
Abstract
Accelerated neurocognitive decline after general anesthesia/surgery, also known as perioperative neurocognitive disorder (PND), is a widely recognized public health problem that may affect millions of patients each year. Advanced age, with its increasing prevalence of heightened stress, inflammation, and neurodegenerative alterations, is a [...] Read more.
Accelerated neurocognitive decline after general anesthesia/surgery, also known as perioperative neurocognitive disorder (PND), is a widely recognized public health problem that may affect millions of patients each year. Advanced age, with its increasing prevalence of heightened stress, inflammation, and neurodegenerative alterations, is a consistent contributing factor to the development of PND. Although a strong homeostatic reserve in young adults makes them more resilient to PND, animal data suggest that young adults with pathophysiological conditions characterized by excessive stress and inflammation may be vulnerable to PND, and this altered phenotype may be passed to future offspring (intergenerational PND). The purpose of this narrative review of data in the literature and the authors’ own experimental findings in rodents is to draw attention to the possibility of intergenerational PND, a new phenomenon which, if confirmed in humans, may unravel a big new population that may be affected by parental PND. In particular, we discuss the roles of stress, inflammation, and epigenetic alterations in the development of PND. We also discuss experimental findings that demonstrate the effects of surgery, traumatic brain injury, and the general anesthetic sevoflurane that interact to induce persistent dysregulation of the stress response system, inflammation markers, and behavior in young adult male rats and in their future offspring who have neither trauma nor anesthetic exposure (i.e., an animal model of intergenerational PND). Full article
(This article belongs to the Special Issue Epigenetic Mechanisms Underlying Brain Development and Neuronal Activity)
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22 pages, 3420 KiB  
Review
Dynamic Regulation of DNA Methylation and Brain Functions
by Jiaxiang Xie, Leijie Xie, Huixian Wei, Xiao-Jiang Li and Li Lin
Biology 2023, 12(2), 152; https://0-doi-org.brum.beds.ac.uk/10.3390/biology12020152 - 18 Jan 2023
Cited by 11 | Viewed by 3205
Abstract
DNA cytosine methylation is a principal epigenetic mechanism underlying transcription during development and aging. Growing evidence suggests that DNA methylation plays a critical role in brain function, including neurogenesis, neuronal differentiation, synaptogenesis, learning, and memory. However, the mechanisms underlying aberrant DNA methylation in [...] Read more.
DNA cytosine methylation is a principal epigenetic mechanism underlying transcription during development and aging. Growing evidence suggests that DNA methylation plays a critical role in brain function, including neurogenesis, neuronal differentiation, synaptogenesis, learning, and memory. However, the mechanisms underlying aberrant DNA methylation in neurodegenerative diseases remain unclear. In this review, we provide an overview of the contribution of 5-methycytosine (5mC) and 5-hydroxylcytosine (5hmC) to brain development and aging, with a focus on the roles of dynamic 5mC and 5hmC changes in the pathogenesis of neurodegenerative diseases, particularly Alzheimer’s disease (AD), Parkinson’s disease (PD), and Huntington’s disease (HD). Identification of aberrant DNA methylation sites could provide potential candidates for epigenetic-based diagnostic and therapeutic strategies for neurodegenerative diseases. Full article
(This article belongs to the Special Issue Epigenetic Mechanisms Underlying Brain Development and Neuronal Activity)
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