RT Conference Proceedings
T1 Physical interactions between MCM and Rad51 facilitate replication fork lesion bypass and ssDNA gap filling by non-recombinogenic functions
A1 Cabello-Lobato, María J.
A1 González-Garrido, Cristina
A1 Cano-Linares, María I.
A1 Wong, Ronald P.
A1 Yáñez-Vílchez, Aurora
A1 Morillo-Huesca, Macarena
A1 Roldán-Romero, Juan M.
A1 Vicioso, Marta
A1 González-Prieto, Román
A1 Ulrich, Helle D.
A1 Prado, Félix
K1 Cdc7
K1 DNA damage
K1 MCM
K1 Rad51
K1 Rad52
K1 Homologous recombination
K1 Replication
K1 Componente 7 del complejo de mantenimiento de minicromosoma
K1 Daño del ADN
K1 Recombinasa Rad51
K1 Proteína recombinante y reparadora de ADN Rad52
K1 Recombinación homóloga
K1 Replicación
AB The minichromosome maintenance (MCM) helicase physically interacts with the recombination proteins Rad51 and Rad52 from yeast to human cells. We show, in Saccharomyces cerevisiae, that these interactions occur within a nuclease-insoluble scaffold enriched in replication/repair factors. Rad51 accumulates in a MCM- and DNA-binding-independent manner and interacts with MCM helicases located outside of the replication origins and forks. MCM, Rad51, and Rad52 accumulate in this scaffold in G1 and are released during the S phase. In the presence of replication-blocking lesions, Cdc7 prevents their release from the scaffold, thus maintaining the interactions. We identify a rad51 mutant that is impaired in its ability to bind to MCM but not to the scaffold. This mutant is proficient in recombination but partially defective in single-stranded DNA (ssDNA) gap filling and replication fork progression through damaged DNA. Therefore, cells accumulate MCM/Rad51/Rad52 complexes at specific nuclear scaffolds in G1 to assist stressed forks through non-recombinogenic functions.
PB Cell Press
YR 2021
FD 2021-07-27
LK http://hdl.handle.net/10668/3669
UL http://hdl.handle.net/10668/3669
LA en
NO Cabello-Lobato MJ, González-Garrido C, Cano-Linares MI, Wong RP, Yáñez-Vílchez A, Morillo-Huesca M, et al. Physical interactions between MCM and Rad51 facilitate replication fork lesion bypass and ssDNA gap filling by non-recombinogenic functions. Cell Rep. 2021 Jul 27;36(4):109440
DS RISalud
RD Apr 5, 2025