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Hedgehog acts as a morphogen by regulating proteolytic processing and activation of full-length Ci/Gli transcriptional effectors but can pattern Drosophila wing discs normally in the absence of regulated proteolytic processing.

Hedgehog-pathway activation in adjacent epithelial and stromal cells, but not in epithelial or stromal cells alone, enables the generation of functional de novo hair follicles in unwounded adult mouse skin.

Cholesterol regulates cell-cell communication by activating the Hedgehog pathway, a central signaling system in development, regeneration and cancer.

The patched hedgehog receptor inhibits the transmembrane transducer smoothened by reducing the accessibility of cholesterol locally at the membrane of the primary cilium.

Primary cilia of neural crest-derived cells mediate Indian hedgehog-induced signal transduction in the periocular mesenchyme and are required for normal anterior segment development.

Direct interaction between Hedgehog-sending and Hedgehog-receiving cytonemes is a fundamental mechanism for morphogen transfer and gradient establishment.

DYRK2 regulator governs the mammalian ciliogenesis to maintain proper embryogenesis via activation of the Hh signaling during development in vivo.

Large-scale skeletal regeneration requires Hh signaling in Sox9+ lineage cells to coordinate callus formation and bone repair.

The dependence of Nematostella germ cell specification on zygotic Hedgehog pathway activity supports the hypothesis that the eumetazoan common ancestor segregated its germline by inductive signals rather than maternal determinants.

Cholesterol accessibility in the plasma membrane can be controlled by proteins and function as a signaling messenger in cell-cell communication pathways.