Turing patterns: how the fish got its spots

melanomagenesis. However, the finding that G:C to T:A transversions were much less common (<4000) indicates that oxidative DNA damage is a much less common mutation-inducing type of DNA damage in melanomagenesis than pyrimidine dimers. With so much oxidative DNA damage generated by ultraviolet light and in particular by UVA, one may ask why there are not more mutations typical for oxidative DNA damage found in melanoma. While many oxidative DNA lesions are not or only poorly mutagenic, 8-oxoG, the most studied type of oxidative DNA base damage has a clearly established potential to generate mutations. The answer to the question is probably that the frequency of mutation formation at sites of 8-oxoG is much lower than that at sites of pyrimidine dimers. Studying mechanism of mutation formation in primary melanocytes is a very important endeavor and should be investigated, as conducted by Wang et al., at all steps of the photocarcinogenesis cascade, including DNA damage formation, cellular responses to DNA damage, and mutation formation. Differences in any of those steps between melanocytes and other skin cells remain highly plausible. In that regard, the influence of different types of melanin on UVA mutagenesis with pheomelanin as photosensitizer and eumelanin as photoprotector may be worth studying. Current evidence, however, favors a much higher contribution of pyrimidine dimers to mutation formation during melanomagenesis than of oxidative DNA damage. In that regard, at the moment, melanoma does not appear to be different from other types of UV-induced skin cancer.