The nuclear concentration of kin17, a mouse protein that binds to curved DNA, increases during cell proliferation and after UV irradiation

UV-irradiation induces, in mammalian cells, the expressionof a set of genes known as the ‘UV-response’, which maybe reminiscent of the bacterial response, called SOS system.The multifunctional protein RecA controls the expressionof the SOS genes. We report the expression profile of amouse gene conserved among mammals, called Kin17, thatcodes a DNA-binding protein of undetermined biochemicalactivity and which shares epitopes with the bacterial RecAprotein. We demonstrate that the level of Kin17 RNA was5-fold higher in mid-S phase of serum-stimulated BALB/c3T3 fibroblasts than in quiescent cells. Cells in S-phasedisplayed a high level of kin17 protein with a markednuclear localisation. The maximal level of Kin17 RNA wasobserved 18 h after serum stimulation, indicating thatKin17 gene is a new member of the late growth-relatedgenes. The accumulation of kin17 protein during cellproliferation follows the increase in Kin17 RNA and correl-ates with DNA synthesis, which suggests a possible role ofkin17 protein in a transaction related to DNA-replication.In quiescent fibroblasts, a 3-fold increase inKin17 RNAwas seen 13 h after UV irradiation. In parallel, kin17protein accumulated in the nucleus, which suggests thatit might be required after the stress produced by UVirradiation.IntroductionExposure of mammalian cells to UV radiation leads to theformation of DNA-lesions and to structural changes thatperturb DNA metabolism. The constitutive expression of genesinvolved in the nucleotide excision repair system (NER*)allows the efficient removal of the great majority of the UV-induced lesions (1). In addition to the NER system, mammaliancells react to UV-irradiation by inducing the ‘UV-response’,which involves the activation of multiple and complex signaltransduction pathways. The UV-activation of nuclear transcrip-tion factors such as AP-1 and p53 leads to the induction of