DNAreparationssystemen

DNAreparationssystemen, or DNA repair systems, are the cellular networks that detect DNA damage, signal its presence, and restore the integrity of the genome. They mitigate damage from replication errors, environmental mutagens, and normal metabolic processes. The major pathways include direct reversal, base excision repair, nucleotide excision repair, mismatch repair, and double-strand break repair by homologous recombination or non-homologous end joining, with translesion synthesis providing lesion tolerance. These pathways are coordinated by DNA damage sensors such as ATM and ATR and by mediators and effectors that regulate cell cycle checkpoints and, if necessary, apoptosis. In direct reversal, specific enzymes reverse certain modifications; BER fixes small base lesions; NER removes bulky adducts; MMR corrects replication mistakes; HR uses a sister chromatid as a template to faithfully restore sequences around a break, while NHEJ ligates broken ends with minimal homology but may be error-prone. Eukaryotes also deploy translesion polymerases to bypass lesions during replication, tolerating damage at the expense of fidelity. Defects in these systems raise cancer risk and cause genetic disorders, while intact repair is essential for aging and genome stability. In medicine, targeting repair pathways, such as PARP inhibitors in BRCA-mutant cancers, exemplifies a therapeutic approach that exploits repair deficiencies. The DNA damage response integrates repair with cell-cycle control, chromatin remodeling, and signaling networks, reflecting the complexity and essential role of DNAreparationssystemen across organisms.