DNA Repair Mechanisms

This study shows that the nuclear envelope protein Msc1 and the ESCRT-III complex are essential for DNA double-strand break repair during late mitosis and G2/M phases.

The paper shows Pol{theta} is recruited via RAD51 ubiquitylation to resolve clustered ICLs causing replication fork collapse in HR-proficient cells.

The paper presents structures of the yeast clamp loader RFC and shows PCNA facilitates nucleotide exchange by promoting ADP release through subunit separation.

This study identifies XPF in Trypanosoma brucei, shows its role in NER, and demonstrates its involvement in DNA repair and sensitivity to DNA-damaging agents.

This paper shows DNA Polymerase α can replicate through bulky DNA lesions in vitro, but its TLS activity is suppressed by replisome components during normal replication.

This study identifies serine residues in PARP2's N-terminus as targets of automodification, showing their role in PARP2 release from DNA damage sites via PARylation.

This study investigates the real-time kinetics of Twinkle, a human mitochondrial helicase, and identifies regulatory roles of its N-terminal ZBD and C-terminal tail, along with mtSSB interactions.

The paper identifies RIF1-Long as a BRCA1 binding partner that enhances RAD51-dependent repair during DNA replication stress.

The paper identifies Ubp10 as a regulator of de novo telomere addition at SiRTAs, showing its role in suppressing translocations and affecting chromosomal rearrangements in yeast.

This study reveals DNA replication fork stabilization and restart mechanisms using biochemical reconstitution in budding yeast.

This study shows that post-exercise serum enhances DNA repair and reduces DNA damage in colon cancer cells, potentially explaining exercise's protective effect against colorectal cancer.

This study identifies how the DNA damage checkpoint stabilizes replication forks by preventing excess origin firing and fork collapse through the regulation of PCNA and HLTF.

This study uses single-molecule techniques to compare how LIG1 and LIG3 bind and ligate gap and nick DNA substrates, revealing differences in binding dynamics and efficiency.

This study identifies TRIP12 as a regulator of DNA polymerase β involvement in DNA damage response and repair by controlling its trafficking and chromatin loading.

The paper shows senataxin and DNA-PKcs redundantly support NHEJ repair of RAG-induced DSBs during V(D)J recombination, with senataxin's function overlapping with RECQL5 and HLTF.

The paper replicates a 2005 finding that BRIT1/MCPH1 is essential for G2/M checkpoint activation in response to DNA damage, confirming the original conclusion after identifying and correcting a figure duplication error.

The paper identifies UFM1 as a regulator of NHEJ by orchestrating chromatin engagement of core components, linking UFMylation defects to DSB repair defects.

This study shows that MMEJ activity changes with age and varies by tissue in rats, with implications for genomic instability and potential therapeutic targets.

This study shows RNF20-mediated H2B monoubiquitination protects stalled replication forks and promotes their restart by facilitating RAD51 loading and preventing MRE11-mediated degradation.

The paper shows neuronal migration in developing brains causes DNA damage through mechanostress, which is repaired normally but can lead to disease if unresolved.

This study shows NLRP3 promotes homologous recombination by interacting with REV7, enhancing DNA repair and affecting PARP inhibitor sensitivity.

This study shows LSH resolves R-loops in prostate cancer cells, reducing transcription-replication conflicts and DNA damage, and identifies LSH as a potential therapeutic target.

This study reveals how the BRCA2 C-terminal domain reshapes RAD51 dimers to bind B-DNA, promoting replication fork stability over homology-directed repair.

The paper reveals a safety latch mechanism in the DNA-unbound MCM2-7 complex that blocks DNA entry and can be disrupted by mutations, leading to replication defects and DNA damage.

This study uses cryo-EM to reveal the proofreading mechanism of the human Pol ε/PCNA holoenzyme, showing how mismatches are processed with PCNA's influence.

This study investigates the interaction between YoaA-χ helicase and SSB in E. coli, revealing SSB's role in modulating helicase activity and its translocation along ssDNA.

This study shows that the Elg1-RLC complex protects cells from replication stress by unloading PCNA from stalled forks, independent of the Mec1-Rad53 checkpoint pathway.

The paper identifies a missense variant in the XPF-like domain of SHOC1 that disrupts meiotic recombination and causes meiotic arrest by impairing DNA repair and chromatin structure.

This study shows that the KU70 SAP domain is essential for repairing exogenous DNA damage but not for V(D)J recombination or development.

The paper shows MMEJ is selectively active in proliferative tissues and suppressed in post-mitotic tissues, with implications for genomic stability and therapy.