DNA Repair Mechanisms

This study shows RPA is critical for human primosome DNA synthesis across inverted repeats, with a specific winged helix-turn-helix domain enhancing RPA-Pol cooperation and structural integration.

This study shows that SRS2 in Arabidopsis has dual roles in meiotic recombination, both inhibiting and promoting crossover formation.

This study identifies RNF25's role in protecting DNA replication forks from degradation, independent of its ubiquitin signaling functions.

This study identifies Mcm10 and RecQL4 as key proteins that activate the eukaryotic replicative DNA helicase CMG through a coordinated mechanism.

This study identifies RPA as a direct interactor of Mer3/HFM1 helicase, showing its role in enhancing helicase processivity and crossover formation during meiosis.

The paper investigates how DNA polymerases in Paramecium tetraurelia ensure high fidelity during programmed DNA rearrangements by analyzing structural changes in polymerase lambda mutants.

This study shows the DNA replication checkpoint facilitates relocation of collapsed CAG/CTG repeat forks to the nuclear periphery via kinetochore phosphorylation and microtubule recruitment in S. cerevisiae.

This study shows that Dna2 nuclease resolves RNA:DNA hybrids at double-strand breaks, promoting resection and accurate repair.

This study shows that checkpoint override in budding yeast increases fitness by enhancing microhomology-mediated end joining repair.

This study shows that replisome progression through R-loops reverses transcriptional repression and prevents fork stalling by reducing RNAPII density.

The paper uses single-molecule FRET to study exonuclease activity in T4 phage MR complexes, revealing two distinct activity states and their regulation by the Mre11 dimer interface.

This study uses STRIDE to show that AZD1390 delays DSB repair and prevents H2AX phosphorylation in 4T1 cells after X-ray irradiation.

The paper presents CryoEM structures of Rad51 and Dmc1 in ADP-bound states and compares them to ATP-bound filaments, revealing structural transitions linked to ATP hydrolysis and filament disassembly.

This study identifies ASCC3 as a helicase that unwinds DNA at stalled replication forks, promoting fork reversal and preventing genomic instability during replication stress.

The paper investigates how RAD52 and RPA interact to promote inverse RNA strand exchange in DNA repair using NMR and biochemical methods.

The paper shows that prolonged G2/M arrest due to DNA damage leads to aberrant mitoses and cell death via securin accumulation in yeast.

The paper uses live-cell imaging to show DNA damage triggers chromatin unfolding via histone ADP-ribosylation, enabling repair access.

This study shows methylglyoxal mutagenizes single-stranded DNA through Rev1-mediated slippage and mispairing, with mutations enriched in tumor datasets.

The paper investigates BRCA1-linked tandem duplication formation in Brca1-deficient cells and identifies allelic DNA synthesis and template switching as key mechanisms.

This study identifies a CST complex-mediated post-resection NHEJ repair pathway that promotes intermediate deletions while preventing larger deletions and rearrangements.

The paper identifies a high spontaneous mutational load in PBMCs of XP-C patients, linked to specific mutation signatures and replication-dependent mutagenesis.

This paper introduces DNAscent, a nanopore sequencing method to map DNA replication dynamics in fission yeast at single-molecule resolution, revealing replication patterns in centromeres and rDNA.

This study shows that the RecB nuclease domain in E. coli RecBCD regulates DNA binding and base pair melting through allosteric effects and linker interactions.

This study shows PARP1 promotes replication-independent DSB formation after MMS-induced methylation damage through NAD+ consumption and PARylation.

This study shows that RNase H2 upregulation mitigates replication stress caused by oncogenes and chemotherapy, reducing replication fork stalling and RNA:DNA hybrids.

This paper introduces a CRISPR-Cas9-based system to induce controlled DNA double strand breaks (DSBs) in yeast and studies the behavior of the Tel1 kinase in response to these breaks.

This study shows human pol δ holoenzymes can bypass various lesions with insertion and extension efficiencies ranging from 0 to 100%.

The paper shows FBH1 limits PRIMPOL-mediated DNA synthesis at stalled replication forks but PRIMPOL does not prevent double strand break formation in FBH1 knockout cells.

The paper shows that DSBs in LADs cause megabase-scale detachment from the nuclear lamina, which is necessary for efficient repair.