Store-Operated Ca2+ Entry in Oocytes Modulate the Dynamics of IP3 -Dependent Ca2+ Release From Oscillatory to Tonic.

Overview

Ca²⁺ signaling is ubiquitous and mediates various cellular functions encoded in its spatial, temporal, and amplitude features. Here, we investigate the role of store-operated Ca²⁺ entry (SOCE) in regulating the temporal dynamics of Ca²⁺ signals in Xenopus oocytes, which can be either oscillatory or tonic. Oscillatory Ca²⁺ release from intracellular stores is typically observed at physiological agonist concentration. When Ca²⁺ release leads to Ca²⁺ store depletion, this triggers the activation of SOCE that translates into a low-amplitude tonic Ca²⁺ signal. SOCE has also been implicated in fueling Ca²⁺ oscillations when activated at low levels. Here, we show that sustained SOCE activation in the presence of IP₃ to gate IP₃ receptors (IP₃ R) results in a pump-leak steady state across the endoplasmic reticulum (ER) membrane that inhibits Ca²⁺ oscillations and produces a tonic Ca²⁺ signal. Tonic signaling downstream of SOCE activation relies on focal Ca²⁺ entry through SOCE ER-plasma membrane (PM) junctions, Ca²⁺ uptake into the ER, followed by release through open IP₃ Rs at distant sites, a process we refer to as "Ca²⁺ teleporting." Therefore, sustained SOCE activation in the presence of an IP₃ -dependent "leak" pathway at the ER membrane results in a switch from oscillatory to tonic Ca²⁺ signaling. J. Cell. Physiol. 232: 1095-1103, 2017. © 2016 Wiley Periodicals, Inc.