Fig. 8.

Deficiency of Sox11 and Sox4 reduces cell migration and re-epithelialization. a Representative images of keratinocytes at the end point of the migration assay using primary keratinocytes from WT or cKO newborns. n = 3 biological replicates. b Graph quantifying relative areas the cells migrated normalized over control. Data are the mean ± SD. n = 3 biological replicates, with 16–24 fields quantified per replicate. ***p < 0.001 (Student’s two-tailed t-test). c Effect of Sox11 and Sox4 on migration of cells lacking both genes. dcKO keratinocytes were transduced to express luciferase (Luc, control), Sox11, Sox4, or both Sox11 and Sox4. Graph quantifying the relative areas the Dox-treated cells migrated normalized over vehicle controls. n = 2 biological replicates, with 12–20 fields quantified per replicate. Data are the mean ± SD. ***p < 0.001 (Student’s two-tailed t-test). d Images of a nude mouse with grafted skins and the splinted wound healing model. WT and cKO neonatal dorsal skins were grafted onto Nude mice pairwise, and splinted wound was created ten weeks post grafting (4 × 10 mm). e Representative images of epidermal tongues five days post wounding in skin of indicated genotypes. f Graph quantifying the amount of re-epithelialization in cKO skin relative to littermate wild type controls. Data are the mean ± SD. n = 4 Sox4 cKO-control pairs, 6 Sox11 cKO-control pairs, and 6 dcKO-control pairs. **p < 0.01 (Student’s two-tailed t-test). g Venn diagram (left) shows the overlapping of genes upregulated in epidermal cells at E13.5 and adult wounded edge⁴, and downregulated in dcKO keratinocytes. The right diagram shows the overlapping of genes downregulated at the wound edge and at E13.5, and upregulated in dcKO keratinocytes. Epi, epidermis; Der, dermis; Es, eschar; LE, leading edge; GL, granulation layer; der, dermis. Scale bars, 100 µm (a), 200 µm (e). Source data for panels b, c, f, and g are provided as a Source Data file