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Life
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Epigenetics and Nuclear Architecture
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Epigenetics and Nuclear Architecture

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Genetics and Genomics".

Deadline for manuscript submissions: closed (27 May 2022) | Viewed by 9225

Special Issue Editor

Dr. Eva Bartova

E-Mail Website
Guest Editor
Institute of Biophysics of the Czech Academy of Sciences, Královopolská 135, 61265 Brno, Czech Republic
Interests: epigenetic of DNA repair; nuclear architecture and gene expression

Special Issue Information

Dear Colleagues,

It is well known that epigenetic factors, including chromatin regulators, histone modifications, and non-coding RNAs, control biological functions, including replication, transcription, splicing, and DNA damage repair. These nuclear events additionally regulate cell proliferation, differentiation, and organogenesis. Disorders in these functions induce pathophysiological processes and, thus, diseases. A Special Edition of Life, an international peer-review journal, aims to compile a timely collection of chapters covering different aspects of chromatin, nuclear architecture, and epigenetic regulation in normal, cancer, and pluripotent stem cells. The topics will mainly address epigenetic regulation of transcription, splicing, and DNA damage repair, as well as cell differentiation. Attention will also be given to the nuclear arrangement and its regulatory role. The list of authors will include many recognized scientists working in the field of epigenetics, chromatin structure, and nuclear architecture. We believe that this Special Edition will serve as a highly valuable resource for the entire scientific community interested in epigenetics and nuclear architecture.

Dr. Eva Bartova
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. Life 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

  • epigenetics
  • DNA methylation
  • histones
  • non-coding RNAs
  • chromatin
  • cell nucleus

Published Papers (4 papers)

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Research

11 pages, 2698 KiB  
Article
Superstructure Detection in Nucleosome Distribution Shows Common Pattern within a Chromosome and within the Genome
by Sujeet Kumar Mishra, Kunhe Li, Simon Brauburger, Arnab Bhattacherjee, Nestor Norio Oiwa and Dieter W. Heermann
Life 2022, 12(4), 541; https://doi.org/10.3390/life12040541 - 06 Apr 2022
Cited by 2 | Viewed by 1488
Abstract
Nucleosome positioning plays an important role in crucial biological processes such as replication, transcription, and gene regulation. It has been widely used to predict the genome’s function and chromatin organisation. So far, the studies of patterns in nucleosome positioning have been limited to [...] Read more.
Nucleosome positioning plays an important role in crucial biological processes such as replication, transcription, and gene regulation. It has been widely used to predict the genome’s function and chromatin organisation. So far, the studies of patterns in nucleosome positioning have been limited to transcription start sites, CTCFs binding sites, and some promoter and loci regions. The genome-wide organisational pattern remains unknown. We have developed a theoretical model to coarse-grain nucleosome positioning data in order to obtain patterns in their distribution. Using hierarchical clustering on the auto-correlation function of this coarse-grained nucleosome positioning data, a genome-wide clustering is obtained for Candida albicans. The clustering shows the existence beyond hetero- and eu-chromatin inside the chromosomes. These non-trivial clusterings correspond to different nucleosome distributions and gene densities governing differential gene expression patterns. Moreover, these distribution patterns inside the chromosome appeared to be conserved throughout the genome and within species. The pipeline of the coarse grain nucleosome positioning sequence to identify underlying genomic organisation used in our study is novel, and the classifications obtained are unique and consistent. Full article
(This article belongs to the Special Issue Epigenetics and Nuclear Architecture)
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14 pages, 1948 KiB  
Article
Single-Cell Image-Based Analysis Reveals Chromatin Changes during the Acquisition of Tamoxifen Drug Resistance
by Han Zhao, Li F. Lin, Joshua Hahn, Junkai Xie, Harvey F. Holman and Chongli Yuan
Life 2022, 12(3), 438; https://doi.org/10.3390/life12030438 - 17 Mar 2022
Cited by 5 | Viewed by 2047
Abstract
Cancer drug resistance is the leading cause of cancer related deaths. The development of drug resistance can be partially contributed to tumor heterogeneity and epigenetic plasticity. However, the detailed molecular mechanism underlying epigenetic modulated drug resistance remains elusive. In this work, we systematically [...] Read more.
Cancer drug resistance is the leading cause of cancer related deaths. The development of drug resistance can be partially contributed to tumor heterogeneity and epigenetic plasticity. However, the detailed molecular mechanism underlying epigenetic modulated drug resistance remains elusive. In this work, we systematically analyzed epigenetic changes in tamoxifen (Tam) responsive and resistant breast cancer cell line MCF7, and adopted a data-driven approach to identify key epigenetic features distinguishing between these two cell types. Significantly, we revealed that DNA methylation and H3K9me3 marks that constitute the heterochromatin are distinctively different between Tam-resistant and -responsive cells. We then performed time-lapse imaging of 5mC and H3K9me3 features using engineered probes. After Tam treatment, we observed a slow transition of MCF7 cells from a drug-responsive to -resistant population based on DNA methylation features. A similar trend was not observed using H3K9me3 probes. Collectively, our results suggest that DNA methylation changes partake in the establishment of Tam-resistant breast cancer cell lines. Instead of global changes in the DNA methylation level, the distribution of DNA methylation features inside the nucleus can be one of the drivers that facilitates the establishment of a drug resistant phenotype in MCF7. Full article
(This article belongs to the Special Issue Epigenetics and Nuclear Architecture)
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14 pages, 6813 KiB  
Article
B Chromosomes’ Sequences in Yellow-Necked Mice Apodemus flavicollis—Exploring the Transcription
by Marija Rajičić, Alexey Makunin, Tanja Adnađević, Vladimir Trifonov, Mladen Vujošević and Jelena Blagojević
Life 2022, 12(1), 50; https://doi.org/10.3390/life12010050 - 30 Dec 2021
Cited by 1 | Viewed by 1752
Abstract
B chromosomes (Bs) are highly polymorphic additional chromosomes in the genomes of many species. Due to the dispensability of Bs and the lack of noticeable phenotypic effects in their carriers, they were considered genetically inert for a long time. Recent studies on Bs [...] Read more.
B chromosomes (Bs) are highly polymorphic additional chromosomes in the genomes of many species. Due to the dispensability of Bs and the lack of noticeable phenotypic effects in their carriers, they were considered genetically inert for a long time. Recent studies on Bs in Apodemus flavicollis revealed their genetic composition, potential origin, and spatial organization in the interphase nucleus. Surprisingly, the genetic content of Bs in this species is preserved in all studied samples, even in geographically distinct populations, indicating its biological importance. Using RT-PCR we studied the transcription activity of three genes (Rraga, Haus6, and Cenpe) previously identified on Bs in A. flavicollis. We analysed mRNA isolated from spleen tissues of 34 animals harboring different numbers of Bs (0–3).The products of transcriptional activity of the analysed sequences differ in individuals with and without Bs. We recorded B-genes and/or genes from the standard genome in the presence of Bs, showing sex-dependent higher levels of transcriptional activity. Furthermore, the transcriptional activity of Cenpe varied with the age of the animals differently in the group with and without Bs. With aging, the amount of product was only found to significantly decrease in B carriers. The potential biological significance of all these differences is discussed in the paper. Full article
(This article belongs to the Special Issue Epigenetics and Nuclear Architecture)
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16 pages, 24315 KiB  
Article
Localization of METTL16 at the Nuclear Periphery and the Nucleolus Is Cell Cycle-Specific and METTL16 Interacts with Several Nucleolar Proteins
by Lenka Stixová, Denisa Komůrková, Alena Svobodová Kovaříková, Paolo Fagherazzi and Eva Bártová
Life 2021, 11(7), 669; https://doi.org/10.3390/life11070669 - 08 Jul 2021
Cited by 4 | Viewed by 2699
Abstract
METTL16 methyltransferase is responsible for the methylation of N6-adenosine (m6A) in several RNAs. In mouse cells, we showed that the nuclear distribution of METTL16 is cell cycle-specific. In the G1/S phases, METTL16 accumulates to the nucleolus, while in the [...] Read more.
METTL16 methyltransferase is responsible for the methylation of N6-adenosine (m6A) in several RNAs. In mouse cells, we showed that the nuclear distribution of METTL16 is cell cycle-specific. In the G1/S phases, METTL16 accumulates to the nucleolus, while in the G2 phase, the level of METTL16 increases in the nucleoplasm. In metaphase and anaphase, there is a very low pool of the METTL16 protein, but in telophase, residual METTL16 appears to be associated with the newly formed nuclear lamina. In A-type lamin-depleted cells, we observed a reduction of METTL16 when compared with the wild-type counterpart. However, METTL16 does not interact with A-type and B-type lamins, but interacts with Lamin B Receptor (LBR) and Lap2α. Additionally, Lap2α depletion caused METTL16 downregulation in the nuclear pool. Furthermore, METTL16 interacted with DDB2, a key protein of the nucleotide excision repair (NER), and also with nucleolar proteins, including TCOF, NOLC1, and UBF1/2, but not fibrillarin. From this view, the METTL16 protein may also regulate the transcription of ribosomal genes because we observed that the high level of m6A in 18S rRNA appeared in cells with upregulated METTL16. Full article
(This article belongs to the Special Issue Epigenetics and Nuclear Architecture)
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