UV-induced thymine dimer

When ultraviolet light from the sun strikes DNA, its energy can do something very specific and damaging: it makes two neighbouring thymine bases on the same strand bond directly to each other, fusing them into a single rigid unit called a thymine dimer (more generally a pyrimidine dimer, since cytosines can join in too). Imagine two adjacent rungs of the DNA ladder suddenly welded together sideways — the smooth helix now has a stiff kink in it.

That kink is the problem. The fused bases can no longer pair properly with the opposite strand, and the bulky distortion physically blocks the enzymes that copy and read DNA, which stall when they hit it. If a cell tries to replicate past a thymine dimer without fixing it, the copying machinery may guess wrongly at what belongs opposite the damage and introduce mutations — which is the molecular root of sunburn's link to skin cancer.

Cells fight back with repair. Many organisms, though notably not placental mammals like us, carry an enzyme called photolyase that uses visible light to split the dimer back apart directly. Humans instead rely on nucleotide excision repair, which cuts out a short patch of strand containing the dimer and resynthesises it from the intact partner strand. The disease xeroderma pigmentosum, in which this repair pathway is broken, shows the stakes plainly: affected people develop severe sun sensitivity and a greatly raised risk of skin cancer, because their cells cannot clear the thymine dimers that sunlight keeps making.