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Genes
Special Issues
Epigenetic Regulation of Cell Fate
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Epigenetic Regulation of Cell Fate

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Epigenomics".

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 19825

Special Issue Editors

Dr. Anja Knaupp

E-Mail Website
Guest Editor
Department of Anatomy and Developmental Biology and Australian Regenerative Medicine Institute, Monash University, Clayton, VIC 3168, Australia
Interests: epigenetic mechanisms; transcription factor modes of action; regulatory complexes; cell identity; cell fate conversions; stem cells; pluripotency maintenance
Dr. Xiaodong (Ethan) Liu

E-Mail Website
Guest Editor
College of Life Science, Westlake University, Hangzhou 310030, China
Interests: stem cell biology; embryo and embryo models; single cell biology

Special Issue Information

Dear Colleagues,

Activation of specific genes in mammalian cells can trigger a change in cellular identity and underlies many physiological and pathological processes. For example, changes in the gene expression program of stem and progenitor cells can initiate their differentiation into more specialized cell types and hence play an essential role in embryonic development, adult tissue homeostasis, and organ regeneration. These transcriptional changes and the levels of the corresponding gene products are regulated through different epigenetic instructional mechanisms. These include histone modifications, DNA methylation, chromatin accessibility, RNA and protein modifications, and the interaction of various factors, including different regulatory elements, transcription factors, epigenetic regulators, long non-coding RNAs, and microRNAs. However, the epigenetic mechanisms underlying cell fate decisions remain largely unexplored.

This Special Issue invites researchers to contribute original research and review articles discussing the epigenetic control of various cellular conversions (e.g., physiological, pathological, and artificial), advances in technological development for understanding epigenetic control mechanisms, and epigenetic-based strategies to restore normal cellular function.

Dr. Anja Knaupp
Dr. Xiaodong (Ethan) Liu
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. Genes 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 2600 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

  • cell identity
  • cellular conversions
  • reprogramming
  • transdifferentiation
  • chromatin remodeling
  • transcription factors
  • DNA methylation
  • histone modifications
  • RNA methylation
  • stem cell fate decisions
  • computational cell biology
  • epigenome engineering
  • single cell biology

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Published Papers (5 papers)

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Research

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28 pages, 5300 KiB  
Article
Embryonic Stem Cell-Derived Neurons as a Model System for Epigenome Maturation during Development
by Sally Martin, Daniel Poppe, Nelly Olova, Conor O’Leary, Elena Ivanova, Jahnvi Pflueger, Jennifer Dechka, Rebecca K. Simmons, Helen M. Cooper, Wolf Reik, Ryan Lister and Ernst J. Wolvetang
Genes 2023, 14(5), 957; https://doi.org/10.3390/genes14050957 - 22 Apr 2023
Cited by 3 | Viewed by 3141
Abstract
DNA methylation in neurons is directly linked to neuronal genome regulation and maturation. Unlike other tissues, vertebrate neurons accumulate high levels of atypical DNA methylation in the CH sequence context (mCH) during early postnatal brain development. Here, we investigate to what extent neurons [...] Read more.
DNA methylation in neurons is directly linked to neuronal genome regulation and maturation. Unlike other tissues, vertebrate neurons accumulate high levels of atypical DNA methylation in the CH sequence context (mCH) during early postnatal brain development. Here, we investigate to what extent neurons derived in vitro from both mouse and human pluripotent stem cells recapitulate in vivo DNA methylation patterns. While human ESC-derived neurons did not accumulate mCH in either 2D culture or 3D organoid models even after prolonged culture, cortical neurons derived from mouse ESCs acquired in vivo levels of mCH over a similar time period in both primary neuron cultures and in vivo development. mESC-derived neuron mCH deposition was coincident with a transient increase in Dnmt3a, preceded by the postmitotic marker Rbfox3 (NeuN), was enriched at the nuclear lamina, and negatively correlated with gene expression. We further found that methylation patterning subtly differed between in vitro mES-derived and in vivo neurons, suggesting the involvement of additional noncell autonomous processes. Our findings show that mouse ESC-derived neurons, in contrast to those of humans, can recapitulate the unique DNA methylation landscape of adult neurons in vitro over experimentally tractable timeframes, which allows their use as a model system to study epigenome maturation over development. Full article
(This article belongs to the Special Issue Epigenetic Regulation of Cell Fate)
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22 pages, 16159 KiB  
Article
TNC Accelerates Hypoxia-Induced Cardiac Injury in a METTL3-Dependent Manner
by Hao Cheng, Linnan Li, Junqiang Xue, Jianying Ma and Junbo Ge
Genes 2023, 14(3), 591; https://doi.org/10.3390/genes14030591 - 26 Feb 2023
Cited by 13 | Viewed by 2460
Abstract
Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a [...] Read more.
Cardiac fibrosis and cardiomyocyte apoptosis are reparative processes after myocardial infarction (MI), which results in cardiac remodeling and heart failure at last. Tenascin-C (TNC) consists of four distinct domains, which is a large multimodular glycoprotein of the extracellular matrix. It is also a key regulator of proliferation and apoptosis in cardiomyocytes. As a significant m6A regulator, METTL3 binds m6A sites in mRNA to control its degradation, maturation, stabilization, and translation. Whether METTL3 regulates the occurrence and development of myocardial infarction through the m6A modification of TNC mRNA deserves our study. Here, we have demonstrated that overexpression of METTL3 aggravated cardiac dysfunction and cardiac fibrosis after 4 weeks after MI. Moreover, we also demonstrated that TNC resulted in cardiac fibrosis and cardiomyocyte apoptosis after MI. Mechanistically, METTL3 led to enhanced m6A levels of TNC mRNA and promoted TNC mRNA stability. Then, we mutated one m6A site “A” to “T”, and the binding ability of METTL3 was reduced. In conclusion, METTL3 is involved in cardiac fibrosis and cardiomyocyte apoptosis by increasing m6A levels of TNC mRNA and may be a promising target for the therapy of cardiac fibrosis after MI. Full article
(This article belongs to the Special Issue Epigenetic Regulation of Cell Fate)
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15 pages, 5104 KiB  
Article
Gene Regulatory Interactions at Lamina-Associated Domains
by Julia Madsen-Østerbye, Mohamed Abdelhalim, Sarah Hazell Pickering and Philippe Collas
Genes 2023, 14(2), 334; https://doi.org/10.3390/genes14020334 - 28 Jan 2023
Cited by 4 | Viewed by 4123
Abstract
The nuclear lamina provides a repressive chromatin environment at the nuclear periphery. However, whereas most genes in lamina-associated domains (LADs) are inactive, over ten percent reside in local euchromatic contexts and are expressed. How these genes are regulated and whether they are able [...] Read more.
The nuclear lamina provides a repressive chromatin environment at the nuclear periphery. However, whereas most genes in lamina-associated domains (LADs) are inactive, over ten percent reside in local euchromatic contexts and are expressed. How these genes are regulated and whether they are able to interact with regulatory elements remain unclear. Here, we integrate publicly available enhancer-capture Hi-C data with our own chromatin state and transcriptomic datasets to show that inferred enhancers of active genes in LADs are able to form connections with other enhancers within LADs and outside LADs. Fluorescence in situ hybridization analyses show proximity changes between differentially expressed genes in LADs and distant enhancers upon the induction of adipogenic differentiation. We also provide evidence of involvement of lamin A/C, but not lamin B1, in repressing genes at the border of an in-LAD active region within a topological domain. Our data favor a model where the spatial topology of chromatin at the nuclear lamina is compatible with gene expression in this dynamic nuclear compartment. Full article
(This article belongs to the Special Issue Epigenetic Regulation of Cell Fate)
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Review

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16 pages, 1053 KiB  
Review
Epigenetic Control of Cell Potency and Fate Determination during Mammalian Gastrulation
by Adrienne E. Sullivan
Genes 2023, 14(6), 1143; https://doi.org/10.3390/genes14061143 - 25 May 2023
Cited by 2 | Viewed by 5025
Abstract
Pluripotent embryonic stem cells have a unique and characteristic epigenetic profile, which is critical for differentiation to all embryonic germ lineages. When stem cells exit the pluripotent state and commit to lineage-specific identities during the process of gastrulation in early embryogenesis, extensive epigenetic [...] Read more.
Pluripotent embryonic stem cells have a unique and characteristic epigenetic profile, which is critical for differentiation to all embryonic germ lineages. When stem cells exit the pluripotent state and commit to lineage-specific identities during the process of gastrulation in early embryogenesis, extensive epigenetic remodelling mediates both the switch in cellular programme and the loss of potential to adopt alternative lineage programmes. However, it remains to be understood how the stem cell epigenetic profile encodes pluripotency, or how dynamic epigenetic regulation helps to direct cell fate specification. Recent advances in stem cell culture techniques, cellular reprogramming, and single-cell technologies that can quantitatively profile epigenetic marks have led to significant insights into these questions, which are important for understanding both embryonic development and cell fate engineering. This review provides an overview of key concepts and highlights exciting new advances in the field. Full article
(This article belongs to the Special Issue Epigenetic Regulation of Cell Fate)
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18 pages, 1152 KiB  
Review
Understanding HAT1: A Comprehensive Review of Noncanonical Roles and Connection with Disease
by Miguel A. Ortega, Diego De Leon-Oliva, Cielo Garcia-Montero, Oscar Fraile-Martinez, Diego Liviu Boaru, María del Val Toledo Lobo, Ignacio García-Tuñón, Mar Royuela, Natalio García-Honduvilla, Julia Bujan, Luis G. Guijarro, Melchor Alvarez-Mon and Miguel Ángel Alvarez-Mon
Genes 2023, 14(4), 915; https://doi.org/10.3390/genes14040915 - 14 Apr 2023
Cited by 10 | Viewed by 4192
Abstract
Histone acetylation plays a vital role in organizing chromatin, regulating gene expression and controlling the cell cycle. The first histone acetyltransferase to be identified was histone acetyltransferase 1 (HAT1), but it remains one of the least understood acetyltransferases. HAT1 catalyzes the acetylation of [...] Read more.
Histone acetylation plays a vital role in organizing chromatin, regulating gene expression and controlling the cell cycle. The first histone acetyltransferase to be identified was histone acetyltransferase 1 (HAT1), but it remains one of the least understood acetyltransferases. HAT1 catalyzes the acetylation of newly synthesized H4 and, to a lesser extent, H2A in the cytoplasm. However, 20 min after assembly, histones lose acetylation marks. Moreover, new noncanonical functions have been described for HAT1, revealing its complexity and complicating the understanding of its functions. Recently discovered roles include facilitating the translocation of the H3H4 dimer into the nucleus, increasing the stability of the DNA replication fork, replication-coupled chromatin assembly, coordination of histone production, DNA damage repair, telomeric silencing, epigenetic regulation of nuclear lamina-associated heterochromatin, regulation of the NF-κB response, succinyl transferase activity and mitochondrial protein acetylation. In addition, the functions and expression levels of HAT1 have been linked to many diseases, such as many types of cancer, viral infections (hepatitis B virus, human immunodeficiency virus and viperin synthesis) and inflammatory diseases (chronic obstructive pulmonary disease, atherosclerosis and ischemic stroke). The collective data reveal that HAT1 is a promising therapeutic target, and novel therapeutic approaches, such as RNA interference and the use of aptamers, bisubstrate inhibitors and small-molecule inhibitors, are being evaluated at the preclinical level. Full article
(This article belongs to the Special Issue Epigenetic Regulation of Cell Fate)
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