Taeyoon Kyung1,7, Sangkyu Lee2,7, Jung Eun Kim1, Taesup Cho2, Hyerim Park1, Yun-Mi Jeong3, Dongkyu Kim1, Anna Shin1, Sungsoo Kim1, Jinhee Baek2,4, Jihoon Kim1, Na Yeon Kim1, Doyeon Woo1, Sujin Chae5, Cheol-Hee Kim3, Hee-Sup Shin2,4, Yong-Mahn Han1, Daesoo Kim1 & Won Do Heo1,2,5,6
1Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, Republic of Korea. 2Center for Cognition and Sociality, Institute for Basic Science (IBS), Daejeon, Republic of Korea. 3Department of Biology, Chungnam National University, Daejeon, Republic of Korea. 4Department of Bio and Brain Engineering, KAIST, Daejeon, Republic of Korea. 5KAIST Institute for the BioCentury, KAIST, Daejeon, Republic of Korea. 6Cancer Metastasis Control Center, KAIST Institute for the BioCentury, KAIST, Daejeon, Republic of Korea. 7These authors contributed equally to this work.
Correspondence to : Yong-Mahn Han or Daesoo Kim or Won Do Heo
Calcium (Ca2+) signals that are precisely modulated in space and time mediate a myriad of cellular processes, including contraction, excitation, growth, differentiation and apoptosis1. However, study of Ca2+ responses has been hampered by technological limitations of existing Ca2+-modulating tools. Here we present OptoSTIM1, an optogenetic tool for manipulating intracellular Ca2+ levels through activation of Ca2+-selective endogenous Ca2+ release-activated Ca2+ (CRAC) channels. Using OptoSTIM1, which combines a plant photoreceptor2, 3 and the CRAC channel regulator STIM1 (ref. 4), we quantitatively and qualitatively controlled intracellular Ca2+ levels in various biological systems, including zebrafish embryos and human embryonic stem cells. We demonstrate that activating OptoSTIM1 in the CA1 hippocampal region of mice selectively reinforced contextual memory formation. The broad utility of OptoSTIM1 will expand our mechanistic understanding of numerous Ca2+-associated processes and facilitate screening for drug candidates that antagonize Ca2+ signals.