Strand annealing and motor driven activities of SMARCAL1 and ZRANB3 are stimulated by RAD51 and the paralog complex DOI Creative Commons

Swagata Halder,

Lepakshi Ranjha, Angelo Taglialatela

et al.

Nucleic Acids Research, Journal Year: 2022, Volume and Issue: 50(14), P. 8008 - 8022

Published: July 8, 2022

Abstract SMARCAL1, ZRANB3 and HLTF are required for the remodeling of replication forks upon stress to promote genome stability. RAD51, along with RAD51 paralog complex, were also found have recombination-independent functions in fork reversal, yet underlying mechanisms remained unclear. Using reconstituted reactions, we build previous data show that unequal biochemical capacities, explaining why they non-redundant functions. SMARCAL1 uniquely anneals RPA-coated ssDNA, which depends on its direct interaction RPA, but not ATP. ZRANB3, efficiently employ ATPase driven translocase activity rezip RPA-covered bubbled DNA, was proposed mimic elements reversal. In contrast, efficient branch migration occurs downstream remodeling. We low concentrations RAD51B–RAD51C–RAD51D–XRCC2 (BCDX2), directly stimulate motor-driven activities HLTF, interplay is underpinned by physical interactions. Our provide a possible mechanism cellular experiments implicating BCDX2

Language: Английский

The plasticity of DNA replication forks in response to clinically relevant genotoxic stress DOI

Matteo Berti,

David Cortez, Massimo Lopes

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2020, Volume and Issue: 21(10), P. 633 - 651

Published: July 1, 2020

Language: Английский

Citations

277
Hallmarks of DNA replication stress DOI Creative Commons
Sneha Saxena, Lee Zou

Molecular Cell, Journal Year: 2022, Volume and Issue: 82(12), P. 2298 - 2314

Published: June 1, 2022

Language: Английский

Citations

224
R-loop-derived cytoplasmic RNA–DNA hybrids activate an immune response DOI
Magdalena P. Crossley,

Chenlin Song,

M Bocek

et al.

Nature, Journal Year: 2022, Volume and Issue: 613(7942), P. 187 - 194

Published: Dec. 21, 2022

Language: Английский

Citations

169
Temporally distinct post-replicative repair mechanisms fill PRIMPOL-dependent ssDNA gaps in human cells DOI Creative Commons

Stephanie Tirman,

Annabel Quinet, Matthew Wood

et al.

Molecular Cell, Journal Year: 2021, Volume and Issue: 81(19), P. 4026 - 4040.e8

Published: Oct. 1, 2021

Language: Английский

Citations

130
REV1-Polζ maintains the viability of homologous recombination-deficient cancer cells through mutagenic repair of PRIMPOL-dependent ssDNA gaps DOI Creative Commons
Angelo Taglialatela, Giuseppe Leuzzi, Vincenzo Sannino

et al.

Molecular Cell, Journal Year: 2021, Volume and Issue: 81(19), P. 4008 - 4025.e7

Published: Sept. 10, 2021

Language: Английский

Citations

125
Leveraging the replication stress response to optimize cancer therapy DOI
Emily Cybulla, Alessandro Vindigni

Nature reviews. Cancer, Journal Year: 2022, Volume and Issue: 23(1), P. 6 - 24

Published: Nov. 2, 2022

Language: Английский

Citations

70
RAD51 bypasses the CMG helicase to promote replication fork reversal DOI
Wenpeng Liu, Yuichiro Saito,

Jessica Jackson

et al.

Science, Journal Year: 2023, Volume and Issue: 380(6643), P. 382 - 387

Published: April 27, 2023

Replication fork reversal safeguards genome integrity as a replication stress response. DNA translocases and the RAD51 recombinase catalyze reversal. However, it remains unknown why is required what happens to machinery during We find that uses its strand exchange activity circumvent replicative helicase, which bound stalled fork. not for if helicase unloaded. Thus, we propose creates parental duplex behind used substrate by branch migration create reversed structure. Our data explain how while maintaining in position poised restart synthesis complete duplication.

Language: Английский

Citations

48
SMARCAL1 is a dual regulator of innate immune signaling and PD-L1 expression that promotes tumor immune evasion DOI Creative Commons
Giuseppe Leuzzi, Alessandro Vasciaveo, Angelo Taglialatela

et al.

Cell, Journal Year: 2024, Volume and Issue: 187(4), P. 861 - 881.e32

Published: Jan. 31, 2024

Language: Английский

Citations

36
BRCA2 promotes genomic integrity and therapy resistance primarily through its role in homology-directed repair DOI Creative Commons
Pei Xin Lim,

Mahdia Zaman,

Weiran Feng

et al.

Molecular Cell, Journal Year: 2024, Volume and Issue: unknown

Published: Jan. 1, 2024

Language: Английский

Citations

31
APOBEC3A induces DNA gaps through PRIMPOL and confers gap-associated therapeutic vulnerability DOI Creative Commons
Ajinkya S. Kawale, Xiaojuan Ran, Parasvi S. Patel

et al.

Science Advances, Journal Year: 2024, Volume and Issue: 10(3)

Published: Jan. 19, 2024

Mutation signatures associated with apolipoprotein B mRNA editing catalytic polypeptide-like 3A/B (APOBEC3A/B) cytidine deaminases are prevalent across cancers, implying their roles as mutagenic drivers during tumorigenesis and tumor evolution. APOBEC3A (A3A) expression induces DNA replication stress increases the cellular dependency on ataxia telangiectasia Rad3-related (ATR) kinase for survival. Nonetheless, how A3A remains unclear. We show that without slowing forks. find single-stranded (ssDNA) gaps through PrimPol-mediated repriming. A3A-induced ssDNA repaired by multiple pathways involving ATR, RAD51, translesion synthesis. Both ATR inhibition trapping of poly(ADP-ribose) polymerase (PARP) PARP inhibitor impair repair gaps, preferentially killing A3A-expressing cells. When used in combination, inhibitors selectively kill cells synergistically a manner dependent PrimPol-generated gaps. Thus, arises from which confer therapeutic vulnerability to gap-targeted inhibitors.

Language: Английский

Citations

18