Store-operated calcium entry inhibits primary ciliogenesis via the activation of Aurora A.

The primary cilium is an antenna-like organelle protruding from the cell surface that can detect physical and chemical stimuli in the extracellular space to activate specific signaling pathways and downstream gene expressions. Calcium ion (Ca 2+ ) signaling regulates a wide spectrum of cellular processes, including fertilization, proliferation, differentiation, muscle contraction, migration and death. This study investigated the effects of the regulation of cytosolic Ca 2+ levels on ciliogenesis using chemical, genetic and optogenetic approaches. We found that ionomycin-induced Ca 2+ influx inhibited ciliogenesis and Ca 2+ chelator BATPA-AM-induced Ca 2+ depletion promoted ciliogenesis. In addition, store-operated Ca 2+ entry and the endoplasmic reticulum Ca 2+ sensor stromal interaction molecule 1 (STIM1) negatively regulated ciliogenesis. Moreover, an optogenetic platform was used to create different Ca 2+ oscillation patterns by manipulating lighting parameters, including density, frequency, exposure time and duration. Light-activated Ca 2+ -translocating channelrhodopsin (CatCh) is activated by 470-nm blue light to induce Ca 2+ influx. Our results show that high-frequency Ca 2+ oscillations decrease ciliogenesis. Furthermore, the inhibition of cilia formation induced by Ca 2+ may occur via the activation of Aurora kinase A. Cilia not only induce Ca 2+ signaling but also regulate cilia formation by Ca 2+ signaling.