Fig. 4: Spatial distribution and cell state characterization of priming.

a, UMAP of pseudotime trajectory D with timepoint (top) and clusters (bottom). b, Comparison of first and second healing. Left: smoothed relative expression (SRE) of deregulated genes in trajectory D. Clusters and timepoints are indicated above, and transiently induced cell plasticity genes (Supplementary Table 3) are highlighted (black box). Right: average z-score expression of cell plasticity genes (top) and their GO analysis (bottom) as −log₁₀ of the adjusted p-value (AdjP). Dashed line underlines significance. c, Single stack of epidermal whole-mount stained with phalloidin (green) and relative cell segmentation (right) at 0w and distal 8w pw1 at 5 mm from wound bed. d, Quantification of cell shape (phalloidin) as ratio between height and width in Lrig1 GL tdTomato⁺ cells in the INFU. 8w pw1 sample was analysed in wound bed (Wb) and distal areas (Distal 1: 3–5 mm and Distal 2: 5–7 mm from wound bed). n = 3 mice. e, Violin plot of Glut1 expression in cells from clusters 0, 7, 11 and 12 and all the other clusters. Cells are divided by timepoint. f, Quantification of Glut1 level in the INFU at 8w pw1, in Wb, Distal and Ctrl (>2 cm from Wb) (ratio to 0w) (left) and INFU whole-mount pictures (right) are shown. n = 3 (Wb), n = 5 (Distal and Ctrl). g, Time lapse migration assay in vitro. Mean track displacement (μm) of cultured 8w pw1 Glut1⁺ versus Glut1⁻ Lrig1 GL tdTomato⁺ sorted cells. n = 3 mice. P-value from a two-tailed t-test. Data are mean ± s.d. Scale bars: 50 μm (c and f). scRNA-seq data (a, b and e) are the integration of two independent experiments, each of them based on four biological replicates.

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