Fig. 6: Wound-distal primed cells are preserved in ageing.

a, Settings to evaluate long-term priming in Lrig1 GL skin: (−1w) genetic labelling; (0w) injury or not; 40 weeks after labelling, wound on both unwounded (40w) and wounded (40w pw1) mice; 1 week after injury, 1w pw1(40) or 1w pw2(40). b,c, Epidermal whole mounts showing Lrig1 GL tdTomato⁺ cells at wound site at 1w pw1(40) and 1w pw2(40) (b) and quantification of the distance from wound centre, compared with young timepoints (c). n = 6 (1w pw1(40)), n = 8 (1w pw2(40)), n = 13 (1w pw1), n = 14 (1w pw2). d, Number of engaged HFs. n = 6 (1w pw1(40)), n = 7 (1w pw2(40)). e, Ex vivo migration assay. Pictures of Lrig1 GL tdTomato⁺ cells exiting from Distal or Ctrl skin explants collected as Fig. 2c. f,g, scRNA-seq of Lrig1 GL cells at 40w and 40w pw1. UMAP of cells coloured by timepoints (f) or clusters (g). h, Comparison of cell lineages derived from Lrig1 SCs in two old (40w and 40w pw1) and two young (0w and 8w pw1) homeostasis, as ratio between them. i, Violin plot of the average expression of memory GO terms (from Fig. 4b) comparing 40w and 40w pw1. Data are median with 25th and 75th percentiles. n = 10 (40w), n = 32 (40w pw1) cells. j,k, Quantification of cell shape, as height–width ratio (n = 9 (40w), n = 16 (40w pw1_Distal)) (j) and pS6 (n = 6 (40w), n = 10 (40w pw1_Distal)) (k) in INFU at 40w and at 40w pw1 in distal memory areas (Distal 3–7 mm from wound site). l, Density plot for glycolysis gene signature in Lrig1 GL cells from Transition Cluster in old (40w and 40w pw1) and young (0w and 8w pw1) homeostasis. m, Glut1 quantification (left) in the INFU whole mounts (right) at 40w and at 40w pw1 Distal. n = 4 (40w), n = 5 (40w pw1_Distal). scRNA-seq data (f–i) are the integration of two independent experiments, each of them based on four biological replicates. P-value from a two-tailed t-test. Data are mean ± s.d., if not differently indicated. Scale bars: 1 mm (b and e); 50 μm (m).

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