DNA Repair Mechanisms

This study identifies the CHAMP1 complex as a regulator of heterochromatin assembly and replication fork stability, showing its role in preventing genomic instability in cancer cells.

This study identifies FANCD2-FANCI's role in coordinating chromatin openness and cell cycle arrest during DNA double-strand break repair.

The paper uses real-time imaging to study replisome rotation during DNA synthesis, finding that high-speed rotation supports continuous synthesis but reduces processivity and increases polymerase numbers.

This study shows that Msh2 deficiency in mice leads to sensory processing deficits due to TRN dysfunction, including oxidative damage and altered interneuron activity.

This study shows that sister chromatids are resolved early in C. elegans meiosis, and that cohesin activity is required for this resolution, which enables homolog bias in recombination.

This study shows 53BP1 condensates drive NHEJ foci formation and function as bioreactors and insulators to enhance DNA repair and pathway selection.

This study identifies bacterial DNA polymerase I as an efficient reverse transcriptase capable of mediating RNA-templated DNA repair synthesis.

This study shows that Nek1 regulates Rad54 phosphorylation at Ser572 to promote HR in adult mice but not in embryos, with Nek3 and Nek5 compensating in embryonic cells.

The paper investigates CO rates in mice, showing SC length isn't the sole factor, and highlights sex-specific regulation of CO designation.

The paper investigates DNA repair pathways that protect against methylation damage, showing that Mbd4 and MutSα cooperate to prevent spontaneous deamination of 5-methylcytosine.

The paper identifies MAEA as a critical regulator of DNA repair and replication, with loss of function causing developmental delay and neurodevelopmental deficits.

The paper presents a new model for how TIMELESS coordinates its functions at the replication fork and in DNA damage response using a combination of genetic and biochemical approaches.

The paper identifies a delayed mechanism of clastogenesis where unrepaired nucleotide lesions in single-stranded DNA persist through mitosis and generate clastogenic DSBs during the subsequent S phase.

This study investigates the interplay between DNA damage tolerance pathways by comparing PCNA occupancy and RPA/Rad51 exchange at stalled replication sites.

This study investigates the minimal NHEJ system in M. tuberculosis using structural simulations, assays, and single-molecule analysis, revealing Ku-LigD interactions and their impact on enzymatic activity.

The paper shows that MutL activates MPG to generate alkylation damage, contributing to cytotoxicity in MMS treatment.

The paper investigates how DNA double-strand breaks formed during replication are processed, finding asymmetrical resection and different requirements for repair pathways.

The paper investigates the role of POLD3 in Mitotic DNA synthesis (MiDAS) by analyzing mutant HeLa cells, showing that POLD3-PCNA interaction coordinates leading and lagging strand synthesis.

This paper identifies RPRM as a tumor suppressor that inhibits NHEJ repair by promoting DNA-PKcs degradation, enhancing tumor radiosensitivity.

The paper identifies endogenous guanine adducts as drivers of tissue-specific mutagenesis and shows that Polκ and DNA repair mechanisms suppress these mutations.

The paper identifies CDK8 as a third kinase involved in DNA replication origin activation by showing its cooperation with CDC7 and its role in phosphorylating MCM4.

The paper shows that heat stress blocks meiosis in yeast by impairing Holliday junction resolution, dependent on H3K79 methylation and a meiotic recombination checkpoint.

The paper shows that aberrant cohesin function in yeast leads to Mcd1 degradation via E3 ligases, promoting cell lethality through a negative feedback mechanism.

This study identifies a feedback mechanism involving Cdk1/Wee1 signaling that primes and tunes RPA phosphorylation, crucial for cell cycle progression and DNA damage response.

This study investigates how PARP1 binds to DNA breaks and chromatin, revealing that nucleosome unwrapping and allostery influence its affinity and binding dynamics.

The paper compares Rad51 and Dmc1 recombinases using structural and functional analyses to show differences in their interfacial amino acids and evolutionary trajectories.

This study shows HP1 and HP1β promote differential recruitment of HR and NHEJ factors at DSBs, with HP1 phase separation essential for HR recruitment.

This study identifies Praja1 as a DNA damage protector through direct DNA binding, showing its role in DNA repair and resistance to damage in cells and E. coli.

This study shows that CSB-deficient iPSCs have impaired DNA repair and stress responses after BPDE exposure, highlighting CSB's role in genome stability during development.

The paper shows cohesin-driven chromatin loop extrusion facilitates homology search during RAD51-mediated DNA repair in mammalian cells.