The human genome encodes several hundreds of ubiquitin E3 enzymes, most of which have poorly understood biological roles. In search for novel ubiquitin E3 enzymes involved in DNA damage tolerance, we ...

Cohesin-mediated loop extrusion limits sister-fork coupling and tethers nearby replication forks under replication stress, promoting fork reversal and slowing fork progression to safeguard genome...

DNA modifications are central to carcinogenesis, chemotherapy drug action, neurodegeneration, and aging. Here, we present a protocol for click-code-seq, a next-generation sequencing technique for geno...

Segura-Bayona et al. uncover genetically separable ATRX functions that independently safeguard telomeres and genome replication, revealing how CST and 9-1-1 pathways suppress accumulation of toxic sin...

Abstract. The NF-κB signaling pathway is a key driver of inflammation and can be activated by many genotoxic stresses. Yet, the mechanisms by which differe

Advances in genomics, proteomics, and bioinformatics have uncovered the existence of thousands of translated small open reading frames less than 100–150 codons in length that encode microproteins. In ...

Abstract. Apurinic/apyrimidinic (AP) sites are among the most frequent DNA lesions, arising thousands of times per cell each day. These lesions threaten ge

Apurinic/apyrimidinic (AP) sites, also known as abasic sites, are among the most frequent DNA lesions, arising spontaneously or as intermediates in base excision repair. Their structural impediment to...

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Replicative single-stranded DNA gaps arise when DNA synthesis proceeds past lesions or difficult-to-replicate regions. This review delineates the pathways that generate, stabilize, and process these i...

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The emergence of a chemical system capable of self-replication and evolution is a critical event in the origin of life. RNA polymerase ribozymes can replicate RNA, but their large size and structural ...

Re-replication is a driving force of tumorigenesis and genomic instability. Here, the authors show that upon re-replication, FANCD2 localizes at early origins to limit replisome progression, ssDNA gap...

Nature Communications - Replication fork plasticity upon genotoxic stress is modulated by nuclear architectural components by elusive mechanisms. Here the authors implicate Lamin A/C – best...

Pathogenic BRCA2 truncating variants in heterozygosis drive distinct cancer-linked mechanisms. Here the authors show that one causes PARPi sensitivity and HR loss via haploinsufficiency, while another...

Cohesin folds genomes into chromatin loops, the roles of which are under debate. We found that double-strand breaks (DSBs) induce de novo formation of chromatin loops in human cells, with the loop bas...

Nature Communications - The study shows that DNA double-strand break repair follows a circadian rhythm: homologous recombination peaks in the morning and declines by evening. CRY1 regulates CCAR2...

Cell Death & Disease - H263A and SCAN1/H493R mutant TDP1 block TOP1-induced double-strand break repair during gene transcription in quiescent cells and promote cell death

Saur, Lesage et al. report that RNA:DNA hybrids arise at double-strand breaks in transcribed genes, independently of de novo recruitment of RNA polymerase II/III, as a result of DSB-induced transcript...

DNA double-strand breaks and unresolved DNA replication intermediates are particularly dangerous during mitosis. Paradoxically, cells inactivate canonical DNA repair mechanisms during chromosome segre...

Incomplete DNA replication and chromosome breakage during mitosis pose major threats to chromosome segregation. The CIP2A-TOPBP1 complex acts to mitigate this peril, but its exact role is not yet unde...

PARP inhibitor treatment triggers histone release from the chromatin in cancer cells; consequently, targeting the histone chaperone NASP renders cells vulnerable to PARP inhibition.

Emerging evidence suggests that, following genotoxic therapy, it is the repair of DNA double-strand breaks, rather than the damage itself, that frequently drives cancer cell death.

Abstract. Replication stress, a hallmark of cancer cells, is detected by checkpoint mechanisms that trigger a range of cellular responses. Among these, the

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Nature - Ku limits RNA-induced innate immunity to allow Alu-expansion in primates

Upon ATR inhibition, APOBEC3B targets unprotected single-stranded DNA at replication forks, leading to fork breakage.

Pioneering research in lung cancer to improve diagnosis, treatment and prevention

HMCES binding to nascent DNA blocks replication and kills homologous recombination–deficient cancer cells.