DNA damage and repair articles from across Nature Portfolio

Chromatin states need to be maintained during DNA damage repair. Here, the authors expand the histone chaperone network involved in repair-coupled chromatin restoration and highlight a mechanistic coordination between old and new histone dynamics.

Diatoms are critical for carbon fixation and have strong biotechnology potential. Here, the authors optimized DNA and protein delivery methods for the model diatom Phaeodactylum tricornutum, also showing that DNA pieces can be stitched together directly in algal cells.

DNA damage stalls RNA polymerase II and halts gene expression. Here, the authors reveal how cells clear stalled polymerase by two hierarchical pathways, in which CSB/CRL4^CSA -triggered ubiquitylation enables rapid TFIIH-driven removal, and with VCP-mediated extraction acting as a backup when this fails.

Acetaldehyde treatment and whole genome sequencing of human cells reveal no increased base substitution mutagenesis but an induction of structural genomic alterations mirrored by the association of similar events with alcohol consumption in cancer.

DNA double-strand breaks are primarily repaired by non-homologous end joining, which requires synapsis of broken DNA ends. Here, the authors show that DNA end configurations, particularly short microhomologies, dictate synaptic complex formation and can bypass XLF to promote close end joining.

Telomeres need to open from a close state which protects the chromosome ends to allow extension by telomerase. Here the authors reveal distinct roles of TPP1 and POT1 in telomerase recruitment and telomere protection using siingle-cell telomerase activity assay.

Precision CRISPR–Cas9-mediated genome engineering remains challenging, particularly gene integration and editing in non-dividing cells. We present Pythia, a deep learning solution that forecasts optimal repair templates and enables predictable and accurate genome editing in diverse cellular contexts, both in vivo and in vitro.

In a recent study published in Nature, Liu, Wang, et al. investigate the mechanisms underlying cytarabine-induced neurotoxicity and provide a mechanistic explanation for the differing neurotoxicity profiles of other nucleoside analogues, such as gemcitabine.

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.

In this Journal Club, Halder and Srivastava discuss a study that investigated how activation-induced deaminase (AID)-mediated DNA double-strand breaks lead to translocations in a cell type-specific manner.