RT Journal Article
T1 Non-Recombinogenic Functions of Rad51, BRCA2, and Rad52 in DNA Damage Tolerance
A1 Prado, Félix
K1 Homologous recombination
K1 Rad51
K1 BRCA2
K1 Rad52
K1 DNA damage tolerance
K1 Recombinación homóloga
K1 Recombinasa Rad51
K1 Proteína BRCA2
K1 Proteína recombinante y reparadora de ADN Rad52
K1 Daño del ADN
AB The DNA damage tolerance (DDT) response is aimed to timely and safely complete DNA replication by facilitating the advance of replication forks through blocking lesions. This process is associated with an accumulation of single-strand DNA (ssDNA), both at the fork and behind the fork. Lesion bypass and ssDNA filling can be performed by translation synthesis (TLS) and template switching mechanisms. TLS uses low-fidelity polymerases to incorporate a dNTP opposite the blocking lesion, whereas template switching uses a Rad51/ssDNA nucleofilament and the sister chromatid to bypass the lesion. Rad51 is loaded at this nucleofilament by two mediator proteins, BRCA2 and Rad52, and these three factors are critical for homologous recombination (HR). Here, we review recent advances showing that Rad51, BRCA2, and Rad52 perform some of these functions through mechanisms that do not require the strand exchange activity of Rad51: the formation and protection of reversed fork structures aimed to bypass blocking lesions, and the promotion of TLS. These findings point to the central HR proteins as potential molecular switches in the choice of the mechanism of DDT.
PB MDPI
YR 2021
FD 2021-09-29
LK http://hdl.handle.net/10668/4226
UL http://hdl.handle.net/10668/4226
LA en
NO Prado F. Non-Recombinogenic Functions of Rad51, BRCA2, and Rad52 in DNA Damage Tolerance. Genes. 2021 Sep 29;12(10):1550
DS RISalud
RD Apr 7, 2025