Exposure to ambient ultraviolet-B (UVB) radiation generates DNA lesions, such as cyclobutane pyrimidine dimers and 6-4 pyrimidine–pyrimidine photoproducts in Tetranychus urticae Koch (Acari: Tetranychidae). Larvae appeared normal and healthy after UVB irradiation. Conversely, many mites were trapped in their old epidermis or experienced retarded development and shrunk, thus failing to molt from protochrysalises to protonymphs and died. This suggested that DNA lesions per se were not causing lethality in mites unless damaged genes were expressed. UVB-induced DNA lesions may have interfered with DNA replication and gene expression during the physiological changes of morphogenesis in the chrysalis stage. Comprehensive gene expression analysis by RNA sequencing revealed that gene expression involving epidermal tissue (characteristically cuticular protein genes) and myosin heavy chain muscle-like genes were downregulated in protochrysalises irradiated with UVB at the larval stage. We conclude that the success of protochrysalis molting is determined by whether the DNA lesions of genes, particularly those connected with morphogenesis, are repaired before expression at the protochrysalis stage.