fig1

Figure 1. Schematic representation of EV-mediated morphogen signaling. A: Wnt ligands localized on the EV surface may bind to Frizzled receptors on a target cell, activating the canonical Wnt pathway. EVs may also contain β-catenin transcription factor or Frizzled receptor, and deliver them to target cells, thus converting them into cells responsive to Wnt pathway activation. Co-receptors are not shown; B: Shh localized on the EV surface may bind to Patched receptor, removing its inhibitory action on Smo receptor. In turn, activated Smo promotes Gli translocation into the nucleus; C: Notch ligands present in the membrane of EVs can bind to Notch receptors localized on the target cell surface (left panel). The presence of unprocessed Notch receptors on ARMMs can lead to the delivery of Notch receptors to the target cell, making it responsive to Notch signaling (right panel); D: EVs may carry either ephrin ligands (A and B), activating forward signaling in target cells expressing Eph receptors (left panel), or Eph receptors, activating reverse signaling in target cells (right panel). EV: Extracellular vesicles; Smo: Smoothened; ARMMs: arrestin domain-containing protein 1-mediated microvesicles; Sufu: suppressor of fused; Shh: sonic Hedgehog.