DNA damage response articles from across Nature Portfolio

How caspases are differentially regulated in non-apoptotic stress responses remains enigmatic. Here, the authors show that Xeroderma pigmentosum protein XPD promotes stress specific caspase expression to balance genotoxic and non-genotoxic responses.

Ubiquitination factors play crucial roles in DNA repair. The authors show that deubiquitinase OTUD5 facilitates ATM-dependent DNA damage signalling via the UBR5-ATMIN axis. OTUD5 loss results in DNA repair defects at heterochromatin and deprotected telomeres due to insufficient KAP1^S824 phosphorylation.

Collisions of transcription and replication machineries on the same DNA strand threaten genomic stability. Here, the authors show that RAD52 prevents these collisions by regulating R-loop formation and resolution. RAD52 deficiency leads to increased R-loops, exacerbated collisions, DNA damage, and higher mutational burden in tumors.

Human cytomegalovirus (HCMV) hijacks host L1 retrotransposon to supercharge its replication. This novel virus-transposon interaction reveals a strategy for viruses to exploit host machinery, accelerating viral DNA replication and enhancing fitness.

Gemcitabine is a widely used chemotherapy drug that acts by targeting DNA replication. Understanding why many tumors are unresponsive to gemcitabine is a clinical challenge. A new study in Nature Cancer reports that upregulation of the cytidine deaminases APOBEC3C and APOBEC3D facilitates resistance to gemcitabine by protecting cells against DNA replication stress.