Figure 4.

Updated model for the translation of FSS to stimulated endocytosis. Our data support a model in which exposure to FSS increases apical endocytic capacity in PT cells via a pathway that requires mechanosensation by the primary cilium. Our previous studies demonstrated that this response requires extracellular Ca²⁺ and is mediated by release of ATP and purinergic receptor (P2R) signaling that leads to release of Ca²⁺ from endoplasmic reticulum (ER) stores. Here we show that FSS‐stimulated endocytosis requires calmodulin (CaM) mediated activation of Cdc42. We hypothesize that Cdc42 modulates cytoskeletal dynamics that lead to increased endocytic capacity.