RAD51 localization and activation following DNA damage
- 29 January 2004
- journal article
- research article
- Published by The Royal Society in Philosophical Transactions Of The Royal Society B-Biological Sciences
- Vol. 359 (1441), 87-93
- https://doi.org/10.1098/rstb.2003.1368
Abstract
The efficient repair of double–strand breaks in DNA is critical for the maintenance of genome stability. In response to ionizing radiation and other DNA–damaging agents, the RAD51 protein, which is essential for homologous recombination, relocalizes within the nucleus to form distinct foci that can be visualized by microscopy and are thought to represent sites where repair reactions take place. The formation of RAD51 foci in response to DNA damage is dependent upon BRCA2 and a series of proteins known as the RAD51 paralogues (RAD51B, RAD51C, RAD51D, XRCC2 and XRCC3), indicating that the components present within foci assemble in a carefully orchestrated and ordered manner. By contrast, RAD51 foci that form spontaneously as cells undergo DNA replication at S phase occur without the need for BRCA2 or the RAD51 paralogues. It is known that BRCA2 interacts directly with RAD51 through a series of degenerative motifs known as the BRC repeats. These interactions modulate the ability of RAD51 to bind DNA. Taken together, these observations indicate that BRCA2 plays a critical role in controlling the actions of RAD51 at both the microscopic (focus formation) and molecular (DNA binding) level.Keywords
This publication has 41 references indexed in Scilit:
- Insights into DNA recombination from the structure of a RAD51–BRCA2 complexNature, 2002
- Recombinational repair and restart of damaged replication forksNature Reviews Molecular Cell Biology, 2002
- Impaired DNA damage-induced nuclear Rad51 foci formation uniquely characterizes Fanconi anemia group D1Oncogene, 2002
- XRCC2 Is a Nuclear RAD51-like Protein Required for Damage-dependent RAD51 Focus Formation without the Need for ATP BindingPublished by Elsevier BV ,2001
- Role of BRCA2 in Control of the RAD51 Recombination and DNA Repair ProteinMolecular Cell, 2001
- A surfeit of RAD51-like genes?Trends in Genetics, 1999
- Centrosome Amplification and a Defective G2–M Cell Cycle Checkpoint Induce Genetic Instability in BRCA1 Exon 11 Isoform–Deficient CellsMolecular Cell, 1999
- Regulation of Rad51 Function by c-Abl in Response to DNA DamageJournal of Biological Chemistry, 1998
- Internal repeats in the BRCA2 protein sequenceNature Genetics, 1996
- Molecular Structure of Nucleic Acids: A Structure for Deoxyribose Nucleic AcidNature, 1953