Defective postreplication repair of UV photoproducts in melanoma: a mutator phenotype

In this issue, the Gabrielli laboratory and collaborators address the bulky CPD lesions created in DNA when UV joins two adjacent pyrimidines (thymine or cytosine), leading to skin cancers such as melanoma (Pavey S et al. (2019) Mol Oncol). Our understanding of postreplication repair mechanisms for bulky lesions has lagged, and the newly reported predominance of translational control in the UV response has important implications. Image taken from Creative Commons Blacklight bulb in ultraviolet by brx0, licensed under CC BY‐SA 2.0. Commentary on