Ca2+ signals initiate at immobile IP3 receptors adjacent to ER-plasma membrane junctions

Nagendra Babu Thillaiappan, Alap P. Chavda, Stephen C. Tovey, David L. Prole () and Colin W. Taylor ()
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Nagendra Babu Thillaiappan: University of Cambridge
Alap P. Chavda: University of Cambridge
Stephen C. Tovey: University of Cambridge
David L. Prole: University of Cambridge
Colin W. Taylor: University of Cambridge

Nature Communications, 2017, vol. 8, issue 1, 1-16

Abstract: Abstract IP3 receptors (IP3Rs) release Ca2+ from the ER when they bind IP3 and Ca2+. The spatial organization of IP3Rs determines both the propagation of Ca2+ signals between IP3Rs and the selective regulation of cellular responses. Here we use gene editing to fluorescently tag endogenous IP3Rs, and super-resolution microscopy to determine the geography of IP3Rs and Ca2+ signals within living cells. We show that native IP3Rs cluster within ER membranes. Most IP3R clusters are mobile, moved by diffusion and microtubule motors. Ca2+ signals are generated by a small population of immobile IP3Rs. These IP3Rs are licensed to respond, but they do not readily mix with mobile IP3Rs. The licensed IP3Rs reside alongside ER-plasma membrane junctions where STIM1, which regulates store-operated Ca2+ entry, accumulates after depletion of Ca2+ stores. IP3Rs tethered close to ER-plasma membrane junctions are licensed to respond and optimally placed to be activated by endogenous IP3 and to regulate Ca2+ entry.

Date: 2017
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DOI: 10.1038/s41467-017-01644-8

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