MIM and Cortactin Antagonism Regulates Ciliogenesis and Hedgehog Signaling

The study explored the role of Missing-in-Metastasis (MIM) in ciliogenesis and Sonic hedgehog (Shh) signaling, which are crucial for hair follicle formation and regeneration. It was found that MIM is essential for maintaining primary cilia and Shh responsiveness in mesenchymal cells. MIM knockdown resulted in increased Src kinase activity and hyperphosphorylation of Cortactin, an actin regulator. Conversely, inhibiting Src or depleting Cortactin could reverse the cilia defect caused by MIM knockdown. Overexpression of Src or phospho-mimetic Cortactin inhibited ciliogenesis, indicating that MIM promotes ciliogenesis by antagonizing Src-dependent phosphorylation of Cortactin. The study also demonstrated that MIM is necessary in the dermal papilla for primary cilia formation and hair follicle regeneration, suggesting a link between MIM and an actin regulatory pathway that controls ciliogenesis and Shh signaling. The number of subjects or the scale of the study was not mentioned, as the research focused on cellular and molecular mechanisms rather than clinical trials or population-based studies.