| Summary: | <i>Prdm1</i> mutant mice are one of the rare mutant strains that do not develop whisker hair follicles while still displaying a pelage. Here, we show that <i>Prdm1</i> is expressed at the earliest stage of whisker development in clusters of mesenchymal cells before placode formation. Its conditional knockout in the murine soma leads to the loss of expression of <i>Bmp2</i>, <i>Shh</i>, <i>Bmp4</i>, <i>Krt17</i>, <i>Edar</i>, and <i>Gli1</i>, though leaving the β-catenin-driven first dermal signal intact. Furthermore, we show that <i>Prdm1</i> expressing cells not only act as a signaling center but also as a multipotent progenitor population contributing to the several lineages of the adult whisker. We confirm by genetic ablation experiments that the absence of macro vibrissae reverberates on the organization of nerve wiring in the mystacial pads and leads to the reorganization of the barrel cortex. We demonstrate that <i>Lef1</i> acts upstream of <i>Prdm1</i> and identify a primate-specific deletion of a <i>Lef1</i> enhancer named Leaf. This loss may have been significant in the evolutionary process, leading to the progressive defunctionalization and disappearance of vibrissae in primates.
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