DNA in 3R: Repair, Replication, and Recombination
1Group of Genome Expression and Repair, IGBMC, 67404 Illkirch Cedex, CU Strasbourg, France
2Group of Molecular Biology of B Cells, IGBMC, 67404 Illkirch Cedex, CU Strasbourg, France
3Group of Transcription and DNA Repair, IPBS, 205 route de Narbonne, 31077 Toulouse, France
4Department of Dermatology, Eberhard Karls University, 72076 Tuebingen, Germany
DNA in 3R: Repair, Replication, and Recombination
Description
DNA is continuously exposed to a range of damaging agents, including reactive cellular metabolites, environmental chemicals, ionizing radiation, and UV light. The biochemical consequences of DNA lesions are diverse and range from obstruction of fundamental cellular pathways like transcription and replication to fixation of mutations. Cellular misfunctioning, cell death, aging, and cancer are the phenotypical consequences of DNA damages accumulation in the genome. Fortunately, an intricate set of genome surveillance mechanisms function to counteract genomic insults. Among these mechanisms, base excision repair (BER) and nucleotide excision repair (NER) are both dedicated to the removal of single-strand lesions contrary to double-strand break repair (DSBR). Additionally, some specialized polymerases can temporarily take over lesion-arrested DNA polymerases during S phase, in a mutagenic mechanism called translesion synthesis (TLS). Such polymerases only work if a more reliable system, such as homologous recombination (HR), cannot avoid stumbled DNA replication. These DNA repair mechanisms function in conjunction with an intricate machinery of damage sensors, responsible of a series of phosphorylations and chromatin modifications that signal to the rest of the cell the presence of lesions on the DNA. Together DNA repair mechanisms and DNA damage signaling systems form a molecular shield against genomic instability called DNA damage response system (DDR). It is of great importance to understand the molecular mechanism that control DDR and concomitantly disclose the spatiotemporal organization of DDR in the context of nuclear architecture.
We invite authors to present both review articles and original research articles that will stimulate the continuing efforts to understand the mechanisms of DNA repair and recombination. Potential topics include, but are not limited to:
- Connection between DNA repair pathways and other fundamental cellular processes such as transcription
- DNA repair and genetic diseases
- DNA repair and aging
- Spatiotemporal organization of the DNA damage response and repair
- Structure-function relationship in DNA repair
- VDJ recombination
Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/mbi/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: