Difficulty: Easy
Correct Answer: Formation of thymine dimers
Explanation:
Introduction:
Ultraviolet radiation from sunlight can induce specific lesions in DNA that disrupt base pairing and replication. Recognizing the signature lesion of UV exposure is fundamental for understanding mutagenesis, DNA repair, and skin cancer biology.
Given Data / Assumptions:
Concept / Approach:
UV photons are absorbed by adjacent pyrimidines in DNA, promoting a photochemical reaction that covalently links them. The dominant products are cyclobutane pyrimidine dimers, especially thymine dimers, and 6 4 photoproducts. These lesions distort the helix and block polymerases unless repaired.
Step-by-Step Solution:
Verification / Alternative check:
Epidemiology and genetics of xeroderma pigmentosum demonstrate the importance of repairing UV induced dimers. Failure to repair leads to high mutation rates and skin cancer susceptibility.
Why Other Options Are Wrong:
Depurination is a spontaneous hydrolytic event not specific to UV. Single strand breaks can occur but are not the hallmark UV lesion. Dehydration is not a DNA lesion. Oxidative 8 oxoG formation is more characteristic of ionizing radiation or reactive oxygen species.
Common Pitfalls:
Confusing UV damage with oxidative stress or ionizing radiation effects. Another pitfall is assuming all DNA damaging agents cause the same predominant lesion.
Final Answer:
Formation of thymine dimers
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