The single best-known molecular signature of ultraviolet injury to DNA is the pyrimidine dimer.
When skin is exposed to UV-B, two adjacent pyrimidine bases on the same strand (classically thymine-thymine) absorb the photon and become covalently joined through a four-membered cyclobutane ring. The resulting cyclobutane pyrimidine dimer (and the related 6-4 photoproduct) kinks the helix and stalls DNA and RNA polymerases.
Cells correct this through nucleotide excision repair, in which a stretch of the damaged strand is excised and resynthesised. Loss of this machinery (as in xeroderma pigmentosum) leaves dimers in place, producing the hallmark C to T mutations of sun-induced skin cancer.
Contrast this with the distractors: cytosine deamination to uracil is a spontaneous hydrolytic mutation, p53 loss and cyclin elevation are downstream cell-cycle effects rather than the direct photochemical lesion.
\[\boxed{\text{UV light } \Rightarrow \text{pyrimidine (thymine) dimers}}\]