Special Issue "DNA Replication"
A special issue of Genes (ISSN 2073-4425).
Deadline for manuscript submissions: closed (30 November 2012)
Prof. Dr. Peter Frank
Department of Medicine I / Institute of Cancer Research, Medical University of Vienna, Borschkegasse 8a, A-1090 Wien, Austria
Phone: +43 1 40160 57529
Fax: +43 1 40160 957500
Interests: enzymology of DNA replication and repair; RNA metabolism; molecular evolution of nucleases
Replication of DNA, even of the simplest one, is a very sophisticated process, depending on a complex enzymatic machinery being evolved over more than a billion of years. The proper action of replication is a prerequisite to maintain the genome integrity of all living organisms and together with other mechanisms it enables the evolution of life. On the one hand the universality of basic principles of duplication, derived from data obtained from the prokaryote kingdom of life, is an undisputed fact in our times. On the other hand the coordination of replication of eukaryotic genomes and the interaction between duplication and the cell division cycle is still a matter of intense research and debate. This special issue intends to demonstrate new developments and concepts in the general field of DNA replication and related topics, e.g. DNA repair. Research or review articles on any topic within the field will be considered. We are looking forward to your contributions.
Prof. Dr. Peter Frank
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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a 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 quarterly 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 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
- eukaryotic DNA replication
- replication fork dynamics
- Okazaki fragments
- DNA polymerases
Concept Paper: Modeling of the SV40 DNA Replication Machine
Genes 2012, 3(4), 742-758; doi:10.3390/genes3040742
Received: 7 October 2012; in revised form: 24 October 2012 / Accepted: 4 November 2012 / Published: 9 November 2012| Download PDF Full-text (5512 KB) | Download XML Full-text
Review: The Replication Fork: Understanding the Eukaryotic Replication Machinery and the Challenges to Genome Duplication
Genes 2013, 4(1), 1-32; doi:10.3390/genes4010001
Received: 3 December 2012; in revised form: 21 January 2013 / Accepted: 22 January 2013 / Published: 29 January 2013| Download PDF Full-text (681 KB) | Download XML Full-text
Article: A Novel Function for the Conserved Glutamate Residue in the Walker B Motif of Replication Factor C
Genes 2013, 4(2), 134-151; doi:10.3390/genes4020134
Received: 8 January 2013; in revised form: 19 March 2013 / Accepted: 20 March 2013 / Published: 26 March 2013| Download PDF Full-text (407 KB) | Download XML Full-text
Genes 2013, 4(2), 198-225; doi:10.3390/genes4020198
Received: 25 March 2013; in revised form: 5 April 2013 / Accepted: 9 April 2013 / Published: 17 April 2013| Download PDF Full-text (1285 KB) | Download XML Full-text | Supplementary Files
Genes 2013, 4(3), 388-434; doi:10.3390/genes4030388
Received: 7 May 2013; in revised form: 30 July 2013 / Accepted: 2 August 2013 / Published: 19 August 2013| Download PDF Full-text (2237 KB) | Download XML Full-text
The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.
Type of Paper: Review
Title: Cellular Responses to Replication Stress: Implications in Cancer Biology and Therapy
Authors: Hui-Ju Hsieh and Guang Peng
Affiliation: Department of Clinical Cancer Prevention, University of Texas MD Anderson Cancer Center, Unit 1013, 6767 Bertner Avenue, Houston, Texas, 77030, USA; E-Mail: email@example.com
Abstract: Replication stress is a characteristic feature of cancer cells, which is often resulted from excessive growth signaling induced by activation of oncogenes or loss of tumor suppressors. In precancerous and cancerous cells, replication stress primarily manifests as a high level of DNA double-strand breaks (DSBs) due to stalling and collapse of DNA replication forks. A key question remains unanswered: how do these cells survive with extensive DSBs caused by replication stress. In this review, we discuss cellular responses to replication stress including replication stress signaling, cell cycle checkpoint regulation, repair of replication lesions and the implications of these replication stress responses in cancer biology and therapy.
Type of Paper: Article
Title: Novel Functions for the Conserved Glutamate Residue in the Walker B Motif of Replication Factor C
Authors: Ankita Chiraniya1, Jeff Finkelstein2, Mike O'Donnell2 and Linda B. Bloom1
Affiliations: 1 Department of Biochemistry & Molecular Biology, University of Florida, Gainesville, Fl 32605, USA; E-Mail: firstname.lastname@example.org
2 Howard Hughes Medical Institute and the Rockefeller University, New York, NY 10021, USA
Abstract: Clamp loaders that load sliding clamps for DNA replication and repair are members of the AAA+ superfamily of ATPases. Conserved Walker B sequence elements in this family of ATPases contribute to ATP hydrolysis. Mutation of the Walker B glutamate in each of the four active sites of RFC reduces DNA-dependent ATP hydrolysis activity as expected, but unexpectedly reduce ATP-binding-dependent interactions with the clamp and DNA. A role for the Walker B glutamate in ATP-induced conformational changes in the clamp loader that promote ligand binding is a previously unknown function for this conserved Glu residue.
Type of Paper: Review
Title: The replication fork: understanding the eukaryotic DNA replication machinery and the challenges to genome duplication
Authors: Adam R. Leman and Eishi Noguchi *
Affiliation: Drexel University College of Medicine, Philadelphia, PA 19102, USA; E-Mail: email@example.com
Abstract: Eukaryotic cells must accurately and efficiently duplicate their genomes during each round of the cell cycle. Multiple linear chromosomes, an abundance of regulatory elements, and chromosome packaging are all challenges that eukaryotic DNA replication machinery must successfully overcome. The DNA replication machinery, the “replisome” complex, is composed of many specialized proteins with functions in supporting replication by DNA polymerases. Efficient replisome progression relies on tight coordination between the various factors of the replisome. Further, DNA replication progression must occur even on less than ideal templates at various genomic loci. Here, we describe the functions of the major replisome components, as well as some of the obstacles to efficient DNA replication that they confront. Together, this review summarizes current understanding of the vastly complicated task of replicating eukaryotic DNA.
Type of Paper: Review
Title: Molecular Mechanisms of DNA Replication Checkpoint Cctivation
Authors: Bénedicte Recolin, Siem Van der Laan and Domenico Maiorano
Affiliation: Genome Surveillance and Stability Laboratory, Institute of Human Genetics (IGH), CNRS - UPR 1142, 141 rue de la Cardonille, 34396 MONTPELLIER Cedex 5, France; E-Mail: Domenico.Maiorano@igh.cnrs.fr
Abstract: DNA synthesis is coupled to cell cycle progression. Progression of the replication fork during S-phase is monitored by a feedback mechanism known as S-phase checkpoint. This signalling pathway ensures that DNA synthesis has been completed once and only once in S-phase, before entering cell division. Failure to activate this checkpoint in response to inhibition of DNA synthesis (under replication) or to abnormal replication (over replication), results in chromosome fragmentation, aneuploidy and genomic instability. In this review we will describe the molecular determinants of the S-phase checkpoint in eukaryotic cells and discuss current model of activation of this signalling pathway.
Last update: 23 November 2012