DNAherstelroutes

DNAherstelroutes is a term used to describe the network of cellular pathways that detect and repair DNA damage in order to preserve genome integrity. DNA lesions arise from replication errors, reactive oxygen species, ultraviolet or chemical exposure, and other stresses. The repair system comprises several specialized processes that target different types of damage.

Major repair routes include base excision repair (BER) for small, non-helix-distorting base lesions; nucleotide excision repair (NER) for bulky adducts and UV-induced damage; and mismatch repair (MMR) for replication errors such as base mismatches and small insertions or deletions. Direct reversal repairs specific lesions without removing the base. Double-strand breaks are addressed by homologous recombination (HR), which is largely error-free when a sister chromatid is available, and non-homologous end joining (NHEJ), which directly joins broken ends and can be error-prone. Translesion synthesis allows specialized polymerases to bypass unrepaired lesions at the cost of fidelity, while single-strand break repair overlaps with BER and other pathways.

Repair pathway choice depends on the type of damage and the cell cycle stage, coordinated by sensing and signaling networks that include ATM and ATR kinases and other checkpoint proteins. The DNAherstelroutes form an interconnected and partly redundant system, enabling cells to cope with diverse insults and to maintain genomic stability.

Biological importance of these routes lies in preventing mutations, cancer, and age-related decline. In humans, defects in NER, MMR, or HR cause disorders such as xeroderma pigmentosum, Lynch syndrome, or Fanconi anemia. Research into these routes informs cancer biology and therapies, including exploiting synthetic lethality with DNA repair defects, as seen with PARP inhibitors in BRCA-mutant cancers.