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. 2003 Apr 1;22(7):1665–1675. doi: 10.1093/emboj/cdg142

graphic file with name cdg142f2.jpg

Fig. 2. Loss of HMGN1 leads to UV hypersensitivity. (A–F) Increased sensitivity of Hmgn1–/– mice to UV-B. Histology of skin after cumulative irradiation of 1200 J/m2 UV-B. (A and BHmgn1+/+ mice, (CFHmgn1–/– mice. Note the increased acanthosis (asterisk; compare E and D with F) and hyperkeratosis (arrows) in the epidermis of the Hmgn1–/– mice. (G and H) Impaired UV repair in MEFs lacking HMGN1. (G) Increased UV sensitivity of Hmgn1–/– fibroblasts. Shown is survival 72 h after irradiation with the indicated doses (see Materials and methods). (H) Decreased rate of gene-specific CPD removal in Hmgn1–/– fibroblasts. Shown is the quantitative analysis of Southern blots with probes specific for the Dhfr and Hmgn2 genes as described in Materials and methods. The 0 h point represents the initial lesion frequency. The bar graphs represent the average of three experiments.