Step 1: Understanding the Concept:
Ultraviolet (UV) radiation causes adjacent pyrimidine bases (often thymines) on a DNA strand to covalently bond, forming bulky lesions known as thymine dimers.
Cells utilize specific repair pathways to identify and remove these structural distortions.
Step 2: Detailed Explanation:
Let's evaluate the given repair mechanisms for their relevance to UV damage.
- Nucleotide Excision Repair (NER): This is a highly versatile repair pathway specifically designed to recognize bulky, helix-distorting DNA lesions, such as those caused by UV light.
The mechanism involves excising a short, single-stranded patch of DNA containing the dimer and synthesizing a fresh replacement strand.
In placental mammals (including humans), NER is the primary and essential mechanism for repairing thymine dimers.
- Photoreactivation: This is another mechanism that uses the enzyme photolyase and visible light to directly break the dimer bonds.
However, the option specifies "only", making it incorrect because NER is widely applicable and humans actually lack the photoreactivation pathway entirely.
- Base Excision Repair (BER): This pathway typically repairs small, non-helix-distorting base lesions (like oxidized or deaminated bases), not bulky dimers.
- Mismatch Repair (MMR): This pathway corrects errors introduced during DNA replication, such as mispaired bases, not environmental UV-induced damage.
Step 3: Final Answer:
Nucleotide excision repair is the correct general and human-relevant mechanism for repairing thymine dimers.
Therefore, option (B) is the correct answer.