Final answer:
UV-induced thymine dimers are corrected by photoreactivation, a process where the enzyme photolyase, using energy from visible light, cleaves the bond between dimers. This is an essential repair mechanism for many organisms, but not for placental mammals, including humans, where nucleotide excision repair is used instead.
Step-by-step explanation:
Damage caused by UV light leading to thymine dimers is corrected using photoreactivation, which restores the two original bases by cleaving the bond between them. Photoreactivation is a direct repair mechanism in which the enzyme photolyase recognizes the distortion in the DNA helix caused by thymine dimers and binds to them. Under the presence of visible light, photolyase absorbs the energy required to break the covalent bond between the thymine dimer, restoring the correct structure of the DNA. This process is crucial for organisms that are regularly exposed to ultraviolet radiation. However, it is important to note that while photoreactivation is present in many organisms, it is not present in placental mammals, including humans. In these cases, thymine dimers are typically repaired by nucleotide excision repair (also known as dark repair), where damaged DNA is removed and replaced with the correct nucleotides.