DNA Repair Mechanisms

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

This study shows the SIR complex stabilizes recombination intermediates during break-induced replication, improving repair efficiency and reducing mutagenesis.

This study shows that UPF1 deficiency in cancer cells causes replication stress but also drug resistance by reducing replication fork stalling and DNA repair pathway activation.

This study identifies NYH0002 as a compound that blocks ILF2, leading to DNA breaks and lethality in cancers with specific genetic profiles.

This study investigates how mouse embryonic stem cells respond to DNA replication stress, finding they survive via ATR- and CHK1-dependent mechanisms but lack a strong G2/M checkpoint and repair DNA crosslinks in S phase.

This study shows that hypomorphic Lig4 mutation in mice causes Th1-skewed intestinal inflammation under adaptive immunodeficiency.

This study identifies PPM1D as a regulator of replication fork restart, showing it prevents excessive nucleolytic degradation and facilitates RAD51-dependent restart, with ATM hyper-signaling counteracting PPM1D loss.

This study uses optical tweezers to investigate RecN's interactions with ssDNA and dsDNA, revealing its predominant ssDNA binding and weak dsDNA binding that forms DNA loop-like structures.

The paper shows that Ku is translocated off DNA ends in an ATP-dependent manner requiring MRN and CtIP, distinct from resection, to enable HR.

This study shows that RNase H1 is critical for mitochondrial genome maintenance in B cells but has little effect on nuclear R-loops.

The paper constructs a mutational signature catalogue (MUSIC) by analyzing DSB repair gene knockouts, identifying gene clusters and novel roles in repair pathways.

The paper shows that RNAPII bypassing DNA lesions, regulated by p300, leads to genome instability and reduced cell proliferation.

This study characterizes the Fen1 enzyme in Giardia duodenalis, showing it can cleave bubble DNA and identifies regions responsible for this activity.

The paper shows that Treacle and MDC1 sequentially coordinate nucleolar reorganization and HDR factor recruitment to restrict DNA repair to the nucleolar periphery.

The paper introduces RF-SIRF, a method to measure reversed DNA replication forks with single-cell and spatio-temporal resolution, revealing their accumulation at the nuclear periphery and an epigenetic code for replication stress.

The paper compares DNA repair pathway expression between sharks and rays/skates using transcriptomics, finding higher expression in sharks for four major DNA repair pathways.

This study shows that BTRR complex deficiency increases genomic instability through copy number alterations, enriched at fragile sites, using CRISPR-edited iPSC models.

This study shows that UDG recognizes DNA damage in the nucleosome through strict structural conditions and potential mechanical deformation of DNA.

This paper shows that SEN1 has three distinct roles in yeast meiosis: enabling IME1 gene expression, preventing DNA:RNA hybrid accumulation, and facilitating double strand break repair and chromosome synapsis.

This study shows that CIP2A-TOPBP1 recruits the SMX tri-nuclease complex to resolve mitotic DNA lesions, ensuring genome integrity and survival of BRCA2-deficient cells.

This study shows c-Abl phosphorylates Plk1 to facilitate G2/M checkpoint release, but this process increases micronuclei formation, revealing a trade-off in DDR termination.

This study shows that RNA polymerase II processing prevents DNA damage-induced neuronal and developmental failure in TC-NER defects by enabling backup repair pathways.

This study determines cryo-EM structures of human MRN complex bound to DNA and TRF2, revealing how MRN senses DNA ends and separates sensing from nuclease activity.

This study shows Rad27/FEN1 prevents rDNA instability by processing Okazaki fragments, avoiding copy number changes in yeast.

This study investigates NONO protein-protein interactions in response to DNA damage and finds that etoposide treatment does not significantly alter these interactions.

This paper shows that the TONSL-MMS22L complex and FANCM form an interdependent chromatin complex to resolve replication stress and improve cancer prognosis.

This study shows βTrCP interacts with the MRN complex and enhances its recruitment to chromatin, improving DNA damage repair.

This study investigates how the CMG helicase bypasses DNA-protein crosslinks on the leading strand without requiring additional replisome factors or unfolding the protein adduct.

This study shows NAT10 depletion affects DNA repair proteins and 3D-genome structure but not histone modifications.