The presence of ultraviolet UV radiation can significantly increase the rate of DNA damage. UV radiation, particularly UV-B 280-320 nm and UV-C 100-280 nm , can be absorbed by the DNA molecules, leading to the formation of covalent bonds between adjacent pyrimidine bases such as thymine and cytosine . This results in the formation of cyclobutane pyrimidine dimers CPDs and pyrimidine 6-4 pyrimidone photoproducts 6-4PPs . These DNA lesions can cause distortions in the DNA helix, leading to errors in replication and transcription, which can ultimately result in mutations, cell death, or cancer.To counteract the harmful effects of UV-induced DNA damage, cells have evolved several repair mechanisms:1. Direct reversal: This repair mechanism involves the direct reversal of the DNA damage without the need for a DNA template. An example of this is photoreactivation, where photolyase enzymes use the energy from visible light to break the covalent bonds in CPDs and 6-4PPs, restoring the original DNA structure.2. Base excision repair BER : In this mechanism, specific DNA glycosylases recognize and remove the damaged base, creating an abasic site. An AP endonuclease then cleaves the DNA backbone, and DNA polymerase fills in the gap using the undamaged strand as a template. Finally, DNA ligase seals the nick in the DNA backbone.3. Nucleotide excision repair NER : NER is a more versatile repair mechanism that can recognize and remove a wide range of bulky DNA lesions, including CPDs and 6-4PPs. In this process, a multi-protein complex recognizes the DNA damage, and endonucleases cleave the DNA on either side of the lesion. The damaged segment is then removed, and DNA polymerase fills in the gap using the undamaged strand as a template. DNA ligase then seals the nick in the DNA backbone.4. Mismatch repair MMR : Although not directly involved in repairing UV-induced DNA damage, MMR plays a crucial role in correcting replication errors that may arise due to the presence of unrepaired DNA lesions. MMR proteins recognize and remove the mismatched base, and DNA polymerase fills in the correct base using the undamaged strand as a template.5. Translesion synthesis TLS : TLS is a damage tolerance mechanism that allows DNA replication to proceed past DNA lesions, such as CPDs and 6-4PPs. Specialized TLS DNA polymerases can insert nucleotides opposite the damaged bases, albeit with lower fidelity than the replicative DNA polymerases. This can result in the incorporation of incorrect bases, leading to mutations. However, TLS can prevent replication fork stalling and collapse, which can be more detrimental to the cell.These repair mechanisms work together to maintain the integrity of the DNA and protect cells from the harmful effects of UV radiation. However, if the rate of DNA damage exceeds the capacity of these repair systems, it can lead to the accumulation of mutations and an increased risk of cancer.