This review article discusses the molecular mechanisms of ultraviolet radiation (UVR)-induced DNA damage and repair. UVR, particularly UV-B (280–315 nm), is a potent mutagen and carcinogen that can cause various DNA lesions, including cyclobutane pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and DNA strand breaks. Organisms have evolved several conserved repair mechanisms to counteract these lesions, such as photoreactivation, base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). Additionally, double-strand break repair (DSBR) through homologous recombination and nonhomologous end joining, SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative. The article details the formation and repair of these lesions, the role of specific enzymes, and the impact of UV exposure on different organisms, highlighting the importance of UV-induced DNA damage and repair in maintaining genomic integrity.This review article discusses the molecular mechanisms of ultraviolet radiation (UVR)-induced DNA damage and repair. UVR, particularly UV-B (280–315 nm), is a potent mutagen and carcinogen that can cause various DNA lesions, including cyclobutane pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and DNA strand breaks. Organisms have evolved several conserved repair mechanisms to counteract these lesions, such as photoreactivation, base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). Additionally, double-strand break repair (DSBR) through homologous recombination and nonhomologous end joining, SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative. The article details the formation and repair of these lesions, the role of specific enzymes, and the impact of UV exposure on different organisms, highlighting the importance of UV-induced DNA damage and repair in maintaining genomic integrity.