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

Abstract

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 (Ca2+) 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 Ca2+ levels on ciliogenesis using chemical, genetic, and optogenetic approaches. We found that ionomycin‐induced Ca2+ influx inhibited ciliogenesis and Ca2+ chelator BATPA‐AM‐induced Ca2+ depletion promoted ciliogenesis. In addition, store‐operated Ca2+ entry and the endoplasmic reticulum Ca2+ sensor stromal interaction molecule 1 (STIM1) negatively regulated ciliogenesis. Moreover, an optogenetic platform was used to create different Ca2+ oscillation patterns by manipulating lighting parameters, including density, frequency, exposure time, and duration. Light‐activated Ca2+‐translocating channelrhodopsin (CatCh) is activated by 470‐nm blue light to induce Ca2+ influx. Our results show that high‐frequency Ca2+ oscillations decrease ciliogenesis. Furthermore, the inhibition of cilia formation induced by Ca2+ may occur via the activation of Aurora kinase A. Cilia not only induce Ca2+ signaling but also regulate cilia formation by Ca2+ signaling.