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 ) 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 levels on ciliogenesis using chemical, genetic, and optogenetic approaches. We found that ionomycin-induced Ca influx inhibited ciliogenesis and Ca chelator BATPA-AM-induced Ca depletion promoted ciliogenesis. In addition, store-operated Ca entry and the endoplasmic reticulum Ca sensor stromal interaction molecule 1 (STIM1) negatively regulated ciliogenesis. Moreover, an optogenetic platform was used to create different Ca oscillation patterns by manipulating lighting parameters, including density, frequency, exposure time, and duration. Light-activated Ca -translocating channelrhodopsin (CatCh) is activated by 470-nm blue light to induce Ca influx. Our results show that high-frequency Ca oscillations decrease ciliogenesis. Furthermore, the inhibition of cilia formation induced by Ca may occur via the activation of Aurora kinase A. Cilia not only induce Ca signaling but also regulate cilia formation by Ca signaling.