How Thymine dimer mutations of DNA repaired in Humans?

Thymine dimer mutations caused by UV radiation are primarily repaired through two main pathways: nucleotide excision repair (NER) and photoreactivation (light repair). Nucleotide Excision Repair (NER): This repair mechanism is used by both prokaryotic and eukaryotic cells to correct DNA damage induced by UV light, including thymine dimers. NER involves several steps: Detection: The DNA damage is recognized by a complex of proteins that scan the DNA for irregularities. Excision: Once a thymine dimer is identified, the segment of DNA containing the dimer is unwound and excised by a series of enzymes. This includes endonucleases that make cuts on either side of the damaged DNA, removing a short, single-stranded DNA segment. Synthesis: DNA polymerase fills in the gap with the correct nucleotides by using the undamaged strand as a template. Ligation: DNA ligase seals the newly synthesized DNA into the existing strand, restoring the DNA to its original state. Photoreactivation (Light Repair): This pathway is specific to organisms that are exposed to sunlight and involves a single enzyme, photolyase, which directly reverses the damage: Direct Reversal: Photolyase binds to the thymine dimer and, upon absorption of visible light, catalyzes a reaction that breaks the covalent bonds linking the thymine bases, directly reversing the damage without removing any DNA segment. These repair mechanisms are crucial for maintaining genomic stability and preventing mutations that could lead to diseases such as cancer. While NER is a more universal and versatile repair pathway, photoreactivation offers a quick, energy-efficient means of directly reversing UV-induced damage in organisms equipped with photolyase. Problem: In humans, the primary response to repair thymine dimer damage is: A) Photoreactivation B) Nucleotide excision repair C) Direct reversal by DNA polymerase D) Base excision repair