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DNA repair enzymes are enzymes that recognize and correct physical damage in DNA, caused by exposure to radiation, UV light or reactive oxygen species. The correction of DNA damage alleviates loss of genetic information, generation of double-strand breaks, and DNA crosslinkages. DNA repair enzymes recognize DNA damage or a nearby site, or enable repair.
Here the authors show that PARP2 drives telomere fragility by orchestrating the Break-induced replication (BIR) pathway. This promotes DNA end resection and DNA synthesis via the regulation of POLD3.
In this study, the authors present structures and functional analyses for the RAD51C-XRCC3 tumor suppressor complex, providing insights into recurrent mutations in cancer and Fanconi Anemia patients that uncover distinct DNA replication fork protection, restart and reversal regions.
Aitken et al. have used mutagen-induced liver tumours to trace individual strands of the DNA double helix to which damage occurred and correlate this with mutational patterns to inform upon tumour evolution.
