Excess microtubule and F-Actin formation mediates primary cilia shortening and loss in response to hyperosmotic milieu

The primary cilium is a small organelle protruding from the cell surface and receives signals from the extracellular milieu. While dozens of studies have reported that several genetic factors impair the structure of primary cilia, evidence for environmental stimuli affecting primary cilia structures is limited. Here, we investigated an extracellular stress that affected primary cilia morphology and its underlying mechanisms. Hyperosmotic shock induced reversible shortenings and disassembly of primary cilia in murine intramedullary collecting duct cells. The primary cilia shortening caused by hyperosmotic shock followed delocalization of pericentriolar materials (PCMs). Excessive microtubule and F-actin formation in the cytoplasm coincided with those hyperosmotic shock-induced changes of primary cilia and PCMs. A microtubule-disrupting agent, Nocodazole, prevented the hyperosmotic shock-induced primary cilia disassembly partially, while preventing the delocalization of PCMs almost 100%. An actin polymerization inhibitor, Latrunculin A, also prevented partially the hyperosmotic shock-induced primary cilia shortening and disassembly, while preventing the delocalization of PCMs almost 100%. We demonstrate that hyperosmotic shock induces reversible morphological changes in primary cilia and PCMs in a manner dependent on excessive formation of microtubule and F-actin.