Efficient DNA repair might make possible the longevity of naked mole-rats. However, whether they have distinctive mechanisms to optimize functions of DNA repair suppressors is unclear. We find that na...

Gene regulation is mediated by the co-occupancy of numerous proteins along individual chromatin fibers. However, our tools for deeply profiling how proteins co-occupy individual fibers, especially at ...

Comparative oncology combines evolutionary biology, ecology, veterinary medicine and clinical oncology to better understand cancer, for example, by identifying the molecular and cellular mechanisms underlying the remarkable cancer resistance of some taxa. Therefore, this Perspective by Vincze et al. calls for the increased use of non-conventional model organisms in cancer research to advance cancer prevention and treatment strategies.

Lamin A/C maintains replication fork integrity during mild replication stress by modulating chromatin structure and restraining RECQ1 activity.

Protein poly-ADP-ribosylation (PARylation) is a post-translational modification formed by transferring successive units of ADP-ribose to target protei…

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Chromatin Immunoprecipitation (ChIP) and Co-Immunoprecipitation (CoIP) assays are the most common approaches to characterize the genomic localization and protein interactors, respectively, for a prote...

Insights into how the linker histone H1 promotes chromatin alterations and allows repair of DNA damage are described.

The FANCD2-FANCI heterodimer contributes to DNA repair at interstrand crosslinks and sites of replication stress. This complex has been physically and mechanistically linked to double-strand break (DSB) repair, but its role in that process remains undefined. Here we show that the FANCD2-FANCI heterodimer dynamically interacts with open chromatin regions, including transient, DSB-induced open chromatin, where it can be stabilized by co-activation by the DNA repair kinase ATM and the Fanconi anemia core ubiquitin ligase. The loaded FANCD2-FANCI heterodimer stabilizes open chromatin and promotes resection and loading of RPA through increased association of BRCA1 and BLM. Chromatin-loaded FANCD2-FANCI has a second distinct function promoting a G2 arrest that is dependent on the ATR-CHK1-WEE1 axis. Our results support a two-step genome surveillance model in which FANCD2-FANCI monitors open chromatin sites and is stably loaded to coordinate DNA repair activities in response to signaling from a DNA repair kinase. ### Competing Interest Statement The authors have declared no competing interest.

Replication stress is a key driver of DNA damage and genome instability. Replication stress-induced fork remodelling generates a new DNA end that is vulnerable to the action of nucleases, and which is...

Perturbed DNA replication can lead to incompletely replicated DNA when cells enter mitosis and can interfere with chromosome segregation. Cells therefore require mechanisms to resolve these lesions du...

Phosphatase enzymes are challenging to study due to a lack of specific inhibitors. Here, authors develop a chemical-genetic system to inhibit and characterize a major Ser/Thr phosphatase complex, and ...