The presence of UV rays, specifically UV-B radiation wavelengths between 280-320 nm , can induce the formation of pyrimidine dimers in newly synthesized DNA strands during replication. Pyrimidine dimers are covalent bonds that form between two adjacent pyrimidine bases cytosine and thymine on the same DNA strand. This process is called photochemical reaction or photodimerization.The formation of pyrimidine dimers occurs when the UV-B radiation is absorbed by the DNA molecule, causing the electrons in the pyrimidine bases to become excited. This excitation leads to the rearrangement of the molecular orbitals, which allows the formation of a cyclobutane ring between the adjacent pyrimidines. The most common type of pyrimidine dimer is the cyclobutane pyrimidine dimer CPD , but another type called the 6-4 photoproduct 6-4PP can also form.The presence of pyrimidine dimers in DNA has several consequences:1. Distortion of the DNA helix: The formation of the covalent bond between the adjacent pyrimidines causes a distortion in the DNA helix, which can lead to errors during DNA replication and transcription.2. Replication errors: DNA polymerases may have difficulty bypassing the pyrimidine dimer, leading to replication errors, such as insertions, deletions, or base substitutions.3. Transcription errors: RNA polymerases may also have difficulty bypassing the pyrimidine dimer, leading to errors in the transcription process and the production of faulty proteins.4. Mutations and DNA damage: If left unrepaired, pyrimidine dimers can lead to permanent mutations in the DNA sequence, which can contribute to the development of various diseases, including cancer.Cells have developed several mechanisms to repair pyrimidine dimers and maintain genomic integrity:1. Nucleotide excision repair NER : This is the primary repair mechanism for pyrimidine dimers. NER involves the recognition of the DNA damage, removal of the damaged segment including the dimer , and synthesis of a new DNA strand using the undamaged complementary strand as a template. The process is completed by DNA ligase, which seals the gap in the DNA strand.2. Photoreactivation: This repair mechanism is found in some organisms, such as bacteria and plants, but not in humans. Photoreactivation involves the use of an enzyme called photolyase, which binds to the pyrimidine dimer and absorbs light energy usually from the visible spectrum to break the covalent bond between the pyrimidines, effectively reversing the dimer formation.3. Translesion synthesis TLS : This is a DNA damage tolerance mechanism that allows DNA replication to continue past the pyrimidine dimer. Specialized DNA polymerases, called translesion polymerases, can bypass the dimer and insert nucleotides opposite the damaged bases. However, TLS is error-prone and can lead to mutations.4. Homologous recombination repair HRR : This mechanism is primarily used to repair double-strand breaks in DNA but can also be involved in the repair of pyrimidine dimers. HRR uses a homologous DNA sequence usually from a sister chromatid as a template to repair the damaged DNA strand.In summary, the presence of UV rays can induce the formation of pyrimidine dimers in DNA, leading to distortion of the DNA helix, replication and transcription errors, and potential mutations. Cells employ various repair mechanisms, such as nucleotide excision repair, photoreactivation, translesion synthesis, and homologous recombination repair, to maintain genomic integrity and prevent the harmful consequences of pyrimidine dimers.