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. Author manuscript; available in PMC: 2013 Oct 29.
Published in final edited form as: Nature. 2011 Aug 24;476(7361):10.1038/nature10346. doi: 10.1038/nature10346

Figure 1.

Figure 1

Germ layer restriction of ectoderm/mesoderm during digit tip regeneration. Sections through a distal digit of K14CreERmTmG (a-e), En1CremTmG (f-i) and Prx1CremTmG (j-u) transgenic mice, following three months post-amputation. Ectoderm contributes to epidermis, nail and sweat glands and fails to contribute to mesoderm tissues (a-i). Dashed line outlines the border between epidermis/dermis (d) and nail plate/matrix (e, i). Segregation of ectoderm in En1CremTmG into dorsal and ventral fates; ventral ectoderm contributes to ventral epidermis and sweat glands (f-h, red arrowheads) with no contributions to the dorsal epidermis or hair follicles (f-h, white arrowheads). A partial contribution to nail reveals dorsal and ventral chimeric origins to the nail plate (i). This boundary is shifted compared to the published lineage mapping study, using En1CreER. Lineage tracing of Prx1Cre shows restricted GFP expression to bone, tendon and mesenchyme, with no contribution to ectoderm. Keratin-14 (K14) expression in Prx1CremTmG digits is mutually exclusive from GFP expression. High magnifications of nail (j-m), bone (n-q) and sweat glands (r-u). Dashed lines outline borders between nail plate/matrix (j-m) and epidermis/dermis (n-u). White arrowheads (r-u) shows sweat glands within ventral mesenchyme are GFP negative. bm, bone marrow; sg, sweat glands.