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Store‐Operated Ca 2+ Entry in Oocytes Modulate the Dynamics of IP 3 ‐Dependent Ca 2+ Release From Oscillatory to Tonic
Author(s) -
Courjaret Raphaël,
Dib Maya,
Machaca Khaled
Publication year - 2017
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25513
Subject(s) - tonic (physiology) , endoplasmic reticulum , microbiology and biotechnology , chemistry , intracellular , biophysics , receptor , calcium signaling , signal transduction , stim1 , agonist , endocrinology , biology , biochemistry
Ca 2+ signaling is ubiquitous and mediates various cellular functions encoded in its spatial, temporal, and amplitude features. Here, we investigate the role of store‐operated Ca 2+ entry (SOCE) in regulating the temporal dynamics of Ca 2+ signals in Xenopus oocytes, which can be either oscillatory or tonic. Oscillatory Ca 2+ release from intracellular stores is typically observed at physiological agonist concentration. When Ca 2+ release leads to Ca 2+ store depletion, this triggers the activation of SOCE that translates into a low‐amplitude tonic Ca 2+ signal. SOCE has also been implicated in fueling Ca 2+ oscillations when activated at low levels. Here, we show that sustained SOCE activation in the presence of IP 3 to gate IP 3 receptors (IP 3 R) results in a pump‐leak steady state across the endoplasmic reticulum (ER) membrane that inhibits Ca 2+ oscillations and produces a tonic Ca 2+ signal. Tonic signaling downstream of SOCE activation relies on focal Ca 2+ entry through SOCE ER‐plasma membrane (PM) junctions, Ca 2+ uptake into the ER, followed by release through open IP 3 Rs at distant sites, a process we refer to as “Ca 2+ teleporting.” Therefore, sustained SOCE activation in the presence of an IP 3 ‐dependent “leak” pathway at the ER membrane results in a switch from oscillatory to tonic Ca 2+ signaling. J. Cell. Physiol. 232: 1095–1103, 2017. © 2016 Wiley Periodicals, Inc.