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8.3
5.5
Journals
Biomolecules
Special Issues
Chromosome Maintenance
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Chromosome Maintenance

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (28 February 2017) | Viewed by 41816

Special Issue Editor

Prof. Dr. Rob De Bruin

E-Mail Website
Guest Editor
MRC Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK
Interests: cell cycle regulated transcription and chromosome maintenance

Special Issue Information

Dear Colleagues,

The eukaryotic cell cycle proceeds through tightly regulated transitions to guarantee that specific events take place in an orderly manner to ensure chromosome maintenance. The high frequency of genetic alterations that affect proteins involved in cell cycle control detected in human tumor cells illustrates the importance of this regulation for faithful cell proliferation. Whilst most of these processes are related to the cell cycle we realize now that a much broader cellular controls are involved in chromosome maintenance. This issue intends to showcase up to date reviews about emerging concepts from future leaders in this exciting area of research.

We thus invite submission review manuscripts (although original research manuscripts are welcome as well) that cover any aspect of chromosome maintenance. This could include DNA replication, DNA repair, the mitotic and meiotic cell cycle, cell motility, cancer evolution and nuclear architecture. Many forms of anti-cancer treatment involve inducing chromosome instability, thus insights into the fundamental mechanisms of chromosome maintenance provides novel therapeutic approaches that will aid the diagnosis and treatment of cancer.

We look forward to reading your contributions.

Prof. Dr. Rob de Bruin
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. Biomolecules 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.

Keywords

  • chromosome maintenance
  • DNA replication
  • DNA damage
  • cell cycle checkpoints
  • chromatin structure
  • cell motility
  • cancer evolution
  • nuclear architecture

Published Papers (4 papers)

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Review

16 pages, 1722 KiB  
Review
DOT1L and H3K79 Methylation in Transcription and Genomic Stability
by Katherine Wood, Michael Tellier and Shona Murphy
Biomolecules 2018, 8(1), 11; https://doi.org/10.3390/biom8010011 - 27 Feb 2018
Cited by 133 | Viewed by 12784
Abstract
The organization of eukaryotic genomes into chromatin provides challenges for the cell to accomplish basic cellular functions, such as transcription, DNA replication and repair of DNA damage. Accordingly, a range of proteins modify and/or read chromatin states to regulate access to chromosomal DNA. [...] Read more.
The organization of eukaryotic genomes into chromatin provides challenges for the cell to accomplish basic cellular functions, such as transcription, DNA replication and repair of DNA damage. Accordingly, a range of proteins modify and/or read chromatin states to regulate access to chromosomal DNA. Yeast Dot1 and the mammalian homologue DOT1L are methyltransferases that can add up to three methyl groups to histone H3 lysine 79 (H3K79). H3K79 methylation is implicated in several processes, including transcription elongation by RNA polymerase II, the DNA damage response and cell cycle checkpoint activation. DOT1L is also an important drug target for treatment of mixed lineage leukemia (MLL)-rearranged leukemia where aberrant transcriptional activation is promoted by DOT1L mislocalisation. This review summarizes what is currently known about the role of Dot1/DOT1L and H3K79 methylation in transcription and genomic stability. Full article
(This article belongs to the Special Issue Chromosome Maintenance)
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1488 KiB  
Review
Common Chemical Inductors of Replication Stress: Focus on Cell‐Based Studies
by Eva Vesela, Katarina Chroma, Zsofia Turi and Martin Mistrik
Biomolecules 2017, 7(1), 19; https://doi.org/10.3390/biom7010019 - 21 Feb 2017
Cited by 67 | Viewed by 11920
Abstract
DNA replication is a highly demanding process regarding the energy and material supply and must be precisely regulated, involving multiple cellular feedbacks. The slowing down or stalling of DNA synthesis and/or replication forks is referred to as replication stress (RS). Owing to the [...] Read more.
DNA replication is a highly demanding process regarding the energy and material supply and must be precisely regulated, involving multiple cellular feedbacks. The slowing down or stalling of DNA synthesis and/or replication forks is referred to as replication stress (RS). Owing to the complexity and requirements of replication, a plethora of factors may interfere and challenge the genome stability, cell survival or affect the whole organism. This review outlines chemical compounds that are known inducers of RS and commonly used in laboratory research. These compounds act on replication by direct interaction with DNA causing DNA crosslinks and bulky lesions (cisplatin), chemical interference with the metabolism of deoxyribonucleotide triphosphates (hydroxyurea), direct inhibition of the activity of replicative DNA polymerases (aphidicolin) and interference with enzymes dealing with topological DNA stress (camptothecin, etoposide). As a variety of mechanisms can induce RS, the responses of mammalian cells also vary. Here, we review the activity and mechanism of action of these compounds based on recent knowledge, accompanied by examples of induced phenotypes, cellular readouts and commonly used doses. Full article
(This article belongs to the Special Issue Chromosome Maintenance)
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631 KiB  
Review
Emerging Roles for Ciz1 in Cell Cycle Regulation and as a Driver of Tumorigenesis
by Tekle Pauzaite, Urvi Thacker, James Tollitt and Nikki A. Copeland
Biomolecules 2017, 7(1), 1; https://doi.org/10.3390/biom7010001 - 27 Dec 2016
Cited by 13 | Viewed by 7827
Abstract
Precise duplication of the genome is a prerequisite for the health and longevity of multicellular organisms. The temporal regulation of origin specification, replication licensing, and firing at replication origins is mediated by the cyclin-dependent kinases. Here the role of Cip1 interacting Zinc finger [...] Read more.
Precise duplication of the genome is a prerequisite for the health and longevity of multicellular organisms. The temporal regulation of origin specification, replication licensing, and firing at replication origins is mediated by the cyclin-dependent kinases. Here the role of Cip1 interacting Zinc finger protein 1 (Ciz1) in regulation of cell cycle progression is discussed. Ciz1 contributes to regulation of the G1/S transition in mammalian cells. Ciz1 contacts the pre-replication complex (pre-RC) through cell division cycle 6 (Cdc6) interactions and aids localization of cyclin A- cyclin-dependent kinase 2 (CDK2) activity to chromatin and the nuclear matrix during initiation of DNA replication. We discuss evidence that Ciz1 serves as a kinase sensor that regulates both initiation of DNA replication and prevention of re-replication. Finally, the emerging role for Ciz1 in cancer biology is discussed. Ciz1 is overexpressed in common tumors and tumor growth is dependent on Ciz1 expression, suggesting that Ciz1 is a driver of tumor growth. We present evidence that Ciz1 may contribute to deregulation of the cell cycle due to its ability to alter the CDK activity thresholds that are permissive for initiation of DNA replication. We propose that Ciz1 may contribute to oncogenesis by induction of DNA replication stress and that Ciz1 may be a multifaceted target in cancer therapy. Full article
(This article belongs to the Special Issue Chromosome Maintenance)
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2492 KiB  
Review
Repair of DNA Double-Strand Breaks in Heterochromatin
by Felicity Z. Watts
Biomolecules 2016, 6(4), 47; https://doi.org/10.3390/biom6040047 - 16 Dec 2016
Cited by 20 | Viewed by 8642
Abstract
DNA double-strand breaks (DSBs) are among the most damaging lesions in DNA, since, if not identified and repaired, they can lead to insertions, deletions or chromosomal rearrangements. DSBs can be in the form of simple or complex breaks, and may be repaired by [...] Read more.
DNA double-strand breaks (DSBs) are among the most damaging lesions in DNA, since, if not identified and repaired, they can lead to insertions, deletions or chromosomal rearrangements. DSBs can be in the form of simple or complex breaks, and may be repaired by one of a number of processes, the nature of which depends on the complexity of the break or the position of the break within the chromatin. In eukaryotic cells, nuclear DNA is maintained as either euchromatin (EC) which is loosely packed, or in a denser form, much of which is heterochromatin (HC). Due to the less accessible nature of the DNA in HC as compared to that in EC, repair of damage in HC is not as straightforward as repair in EC. Here we review the literature on how cells deal with DSBs in HC. Full article
(This article belongs to the Special Issue Chromosome Maintenance)
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