The Rad51 and Dmc1 recombinases: a non-identical twin relationship.
A double-strand break in genomic DNA that remains unrepaired can be lethal for a cell. Indeed, the integrity of the genome is paramount for survival. It is therefore surprising that some cells deliberately introduce double-strand breaks at certain times during their life cycle. Why might they do this? What are the benefits? How are these breaks repaired? The answers to these questions lie in understanding the basis of meiotic recombination, the process that leads to genetic variation. This review summarizes the key roles played by the two recombinases, Dmc1 and Rad51, in the faithful repair of DNA breaks.
Masson
J Y
JY
Imperial Cancer Research Fund, Clare Hall Laboratories, South Mimms, EN6 3LD, Herts, UK.
West
S C
SC
D000818:Animals; D018797:Cell Cycle Proteins; D004247:DNA / Q000648:ultrastructure; D004249:DNA Damage; D004260:DNA Repair; D004268:DNA-Binding Proteins / Q000737:chemistry*; D004926:Escherichia coli / Q000201:enzymology; D006801:Humans; D008540:Meiosis; D008957:Models, Genetic; D051135:Rad51 Recombinase; D011995:Recombination, Genetic
D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D004247:DNA; C495153:RAD51 protein, human; D051135:Rad51 Recombinase; C074556:DMC1 protein, human