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Gabriela Morosan-Puopolo, Ajeesh Balakrishnan-Renuka, Faisal Yusuf, Jingchen Chen, Fangping Dai, Georg Zoidl, Timo Hans-Werner Lüdtke, Andreas Kispert, Carsten Theiß, Mohammed Abdelsabour-Khalaf, Beate Brand-Saberi

• The embryonic origin of the dermis in vertebrates can be traced back to the dermomyotome of the somites, the lateral plate mesoderm and the neural crest. The dermal precursors directly overlying the neural tube display a unique dense arrangement and are the first to induce skin appendage formation in vertebrate embryos. These dermal precursor cells have been shown to derive from the dorsomedial lip of the dermomyotome (DML). Based on its expression pattern in the DML, \(\it Wnt11\) is a candidate regulator of dorsal dermis formation. Using EGFP-based cell labelling and time-lapse imaging, we show that the \(\it Wnt11\) expressing DML is the source of the dense dorsal dermis. Loss-of-function studies in chicken embryos show that \(\it Wnt11\) is indeed essential for the formation of dense dermis competent to support cutaneous appendage formation. Our findings show that dermogenic progenitors cannot leave the DML to form dense dorsal dermis following \(\it Wnt11\) silencing. No alterations were noticeable in the patterning or in the epithelial state of the dermomyotome including the DML. Furthermore, we show that \(\it Wnt11\) expression is regulated in a manner similar to the previously described early dermal marker \(\it cDermo-1\). The analysis of Wnt11mutant mice exhibits an underdeveloped dorsal dermis and strongly supports our gene silencing data in chicken embryos. We conclude that Wnt11 is required for dense dermis and subsequent cutaneous appendage formation, by influencing the cell fate decision of the cells in the DML.