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Nuclear Architecture in Differentiation and Diseases
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Nuclear Architecture in Differentiation and Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 April 2022) | Viewed by 28419

Special Issue Editors

Prof. Dr. Hans J. Lipps

E-Mail Website1 Website2
Guest Editor
Prof. em. for Cell Biology Hans J. Lipps, University Witten/Herdecke, 58455 Witten, Germany
Interests: chromosome; telomere; DNA structure; chromatin; epigenetic; ciliates
Prof. Dr. Jan Postberg

E-Mail Website
Guest Editor
1. Children’s Hospital, Center for Clinical and Translational Research (CCTR), Helios University Medical Center Wuppertal, Witten/Herdecke University, 42283 Wuppertal, Germany
2. Laboratory of Clinical Molecular Genetics and Epigenetics, Center for Biomedical Education and Research, School of Life Sciences (ZBAF), Faculty of Health, Witten/Herdecke University, 42283 Wuppertal, Germany
Interests: evolution of nuclear architecture; noncoding RNA and histone variants; viral infections and the host cell nucleus

Special Issue Information

Dear Colleagues,

A major challenge of cell biology in the postgenomic era is to understand how the genome is spatiotemporally organized in the 3D/4D nuclear space of eukaryotic cells and how this organization contributes to essential cellular processes such as gene expression, replication, DNA repair or chromosome segregation.

The analysis of the nuclear architecture is a relatively young field of research, which was driven during the last two decades by revolutionary advances in microscopy and deep sequencing technologies. Many features are still under debate, but we are starting to recognize how an impaired nuclear architecture can cause diseases. Thus, developmental programs are resulting in cell-type-specific 3D/4D nuclear organization of cells, which form tissues and organs within the system of the human body. Some instances have been described of how disruptions of these programs can lead to nuclear organization defects, which can be associated with severe developmental disorders. It is the scope of this Special Issue to present the latest insights into the principles of higher order organization of the genome and the epigenome in the cell nucleus from an evolutionary perspective on diverse taxa toward differential 3D/4D nuclear organization in the multiple cell types of complex organisms, such as mammals. This will contribute to our understanding of basic nuclear processes, but importantly also toward the molecular basis of some human diseases as part of a developing systems medicine perspective.

Prof. Dr. Hans J. Lipps
Prof. Dr. Jan Postberg
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • nuclear structure
  • epigenetics
  • cellular differentiation
  • gene expression
  • replication
  • DNA repair
  • disease

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Published Papers (3 papers)

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Research

17 pages, 2493 KiB  
Article
Hyperglycemia Altered DNA Methylation Status and Impaired Pancreatic Differentiation from Embryonic Stem Cells
by Andy Chun Hang Chen, Wen Huang, Sze Wan Fong, Chris Chan, Kai Chuen Lee, William Shu Biu Yeung and Yin Lau Lee
Int. J. Mol. Sci. 2021, 22(19), 10729; https://doi.org/10.3390/ijms221910729 - 3 Oct 2021
Cited by 8 | Viewed by 2660
Abstract
The prevalence of type 2 diabetes (T2D) is rapidly increasing across the globe. Fetal exposure to maternal diabetes was correlated with higher prevalence of impaired glucose tolerance and T2D later in life. Previous studies showed aberrant DNA methylation patterns in pancreas of T2D [...] Read more.
The prevalence of type 2 diabetes (T2D) is rapidly increasing across the globe. Fetal exposure to maternal diabetes was correlated with higher prevalence of impaired glucose tolerance and T2D later in life. Previous studies showed aberrant DNA methylation patterns in pancreas of T2D patients. However, the underlying mechanisms remained largely unknown. We utilized human embryonic stem cells (hESC) as the in vitro model for studying the effects of hyperglycemia on DNA methylome and early pancreatic differentiation. Culture in hyperglycemic conditions disturbed the pancreatic lineage potential of hESC, leading to the downregulation of expression of pancreatic markers PDX1, NKX6−1 and NKX6−2 after in vitro differentiation. Genome-wide DNA methylome profiling revealed over 2000 differentially methylated CpG sites in hESC cultured in hyperglycemic condition when compared with those in control glucose condition. Gene ontology analysis also revealed that the hypermethylated genes were enriched in cell fate commitment. Among them, NKX6−2 was validated and its hypermethylation status was maintained upon differentiation into pancreatic progenitor cells. We also established mouse ESC lines at both physiological glucose level (PG-mESC) and conventional hyperglycemia glucose level (HG-mESC). Concordantly, DNA methylome analysis revealed the enrichment of hypermethylated genes related to cell differentiation in HG-mESC, including Nkx6−1. Our results suggested that hyperglycemia dysregulated the epigenome at early fetal development, possibly leading to impaired pancreatic development. Full article
(This article belongs to the Special Issue Nuclear Architecture in Differentiation and Diseases)
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20 pages, 3180 KiB  
Article
Aluminum Enters Mammalian Cells and Destabilizes Chromosome Structure and Number
by Mirna R. Tenan, Adeline Nicolle, Daniela Moralli, Emeline Verbouwe, Julia D. Jankowska, Mary-Anne Durin, Catherine M. Green, Stefano J. Mandriota and André-Pascal Sappino
Int. J. Mol. Sci. 2021, 22(17), 9515; https://doi.org/10.3390/ijms22179515 - 1 Sep 2021
Cited by 15 | Viewed by 20919
Abstract
Chromosome instability (CIN) consists of high rates of structural and numerical chromosome abnormalities and is a well-known hallmark of cancer. Aluminum is added to many industrial products of frequent use. Yet, it has no known physiological role and is a suspected human carcinogen. [...] Read more.
Chromosome instability (CIN) consists of high rates of structural and numerical chromosome abnormalities and is a well-known hallmark of cancer. Aluminum is added to many industrial products of frequent use. Yet, it has no known physiological role and is a suspected human carcinogen. Here, we show that V79 cells, a well-established model for the evaluation of candidate chemical carcinogens in regulatory toxicology, when cultured in presence of aluminum—in the form of aluminum chloride (AlCl3) and at concentrations in the range of those measured in human tissues—incorporate the metal in a dose-dependent manner, predominantly accumulating it in the perinuclear region. Intracellular aluminum accumulation rapidly leads to a dose-dependent increase in DNA double strand breaks (DSB), in chromosome numerical abnormalities (aneuploidy) and to proliferation arrest in the G2/M phase of the cell cycle. During mitosis, V79 cells exposed to aluminum assemble abnormal multipolar mitotic spindles and appear to cluster supernumerary centrosomes, possibly explaining why they accumulate chromosome segregation errors and damage. We postulate that chronic aluminum absorption favors CIN in mammalian cells, thus promoting carcinogenesis. Full article
(This article belongs to the Special Issue Nuclear Architecture in Differentiation and Diseases)
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16 pages, 2327 KiB  
Article
LEDGF/p75 Is Required for an Efficient DNA Damage Response
by Victoria Liedtke, Christian Schröder, Dirk Roggenbuck, Romano Weiss, Ralf Stohwasser, Peter Schierack, Stefan Rödiger and Lysann Schenk
Int. J. Mol. Sci. 2021, 22(11), 5866; https://doi.org/10.3390/ijms22115866 - 30 May 2021
Cited by 20 | Viewed by 3931
Abstract
Lens epithelium-derived growth factor splice variant of 75 kDa (LEDGF/p75) plays an important role in cancer, but its DNA-damage repair (DDR)-related implications are still not completely understood. Different LEDGF model cell lines were generated: a complete knock-out of LEDGF (KO) and re-expression of [...] Read more.
Lens epithelium-derived growth factor splice variant of 75 kDa (LEDGF/p75) plays an important role in cancer, but its DNA-damage repair (DDR)-related implications are still not completely understood. Different LEDGF model cell lines were generated: a complete knock-out of LEDGF (KO) and re-expression of LEDGF/p75 or LEDGF/p52 using CRISPR/Cas9 technology. Their proliferation and migration capacity as well as their chemosensitivity were determined, which was followed by investigation of the DDR signaling pathways by Western blot and immunofluorescence. LEDGF-deficient cells exhibited a decreased proliferation and migration as well as an increased sensitivity toward etoposide. Moreover, LEDGF-depleted cells showed a significant reduction in the recruitment of downstream DDR-related proteins such as replication protein A 32 kDa subunit (RPA32) after exposure to etoposide. The re-expression of LEDGF/p75 rescued all knock-out effects. Surprisingly, untreated LEDGF KO cells showed an increased amount of DNA fragmentation combined with an increased formation of γH2AX and BRCA1. In contrast, the protein levels of ubiquitin-conjugating enzyme UBC13 and nuclear proteasome activator PA28γ were substantially reduced upon LEDGF KO. This study provides for the first time an insight that LEDGF is not only involved in the recruitment of CtIP but has also an effect on the ubiquitin-dependent regulation of DDR signaling molecules and highlights the role of LEDGF/p75 in homology-directed DNA repair. Full article
(This article belongs to the Special Issue Nuclear Architecture in Differentiation and Diseases)
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