Mammalian Radiation Sensitive 52 (RAD52) is a gene whose scientific reputation has recently seen a strong resurgence. In the past decade, RAD52, which was thought to be dispensable for most DNA repair and recombination reactions in mammals, has been shown to be important for a bevy of DNA metabolic pathways. One of these processes is termed break-induced replication (BIR), a mechanism that can be used to re-start broken replication forks and to elongate the ends of chromosomes in telomerase-negative cells. Viruses have historically evolved a myriad of mechanisms in which they either conscript cellular factors or, more frequently, inactivate them as a means to enable their own replication and survival. Recent data suggests that Adeno-Associated Virus (AAV) may replicate its DNA in a BIR-like fashion and/or utilize RAD52 to facilitate viral transduction and, as such, likely conscripts/requires the host RAD52 protein to promote its perpetuation.
Bibliographical noteFunding Information:
Funding: Work in the Hendrickson laboratory was supported in part by grants from the NIH (GM088351) and the NCI (CA190492).
© 2020 by the author. Licensee MDPI, Basel, Switzerland.
- Adeno-associated virus
- Alternative non-homologous end joining
- Break-induced replication
- Herpes simplex virus
- Human immunodeficiency virus
- Single-strand annealing