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Despite its importance, the molecular choreography driving these collective cellular behaviors remains poorly understood, posing a major challenge in developmental biology and limiting progress in regenerative medicine. Here, we use the developing mouse hair follicle as a model mini-organ to investigate the early events of epithelial bud formation. We identify the Rho GTPase regulator ARHGEF3 as a critical upstream factor that restricts cell fate acquisition and establishes a radial gradient of P-cadherin across the placode during early hair follicle development. In\n                    <jats:italic>Arhgef3<\/jats:italic>\n                    knockout embryos, placodes are enlarged and exhibit elevated P-cadherin levels at cell-cell junctions, disrupting gradient formation without affecting E-cadherin distribution. This defect correlates with aberrant epithelial organization and increased incidence of straight hair follicle downgrowth. Our findings position ARHGEF3 as a novel regulator of cadherin patterning and placode polarization, and suggest broader roles in the morphogenesis of other epithelial appendages governed by similar developmental programs.\n                  <\/jats:p>","DOI":"10.1371\/journal.pbio.3003572","type":"journal-article","created":{"date-parts":[[2026,1,5]],"date-time":"2026-01-05T18:24:16Z","timestamp":1767637456000},"page":"e3003572","update-policy":"https:\/\/doi.org\/10.1371\/journal.pbio.corrections_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Rho GTPase regulator ARHGEF3 orchestrates hair placode budding by coordinating cell fate and P-cadherin patterning in 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