%0 Journal Article
%T TRIC-A shapes oscillatory Ca2+ signals by interaction with STIM1/Orai1 complexes
%A Bernadett Bacsa
%A Helmut Bischof
%A Hwei Ling Ong
%A Indu Suresh Ambudkar
%A Klaus Groschner
%A Niroj Shrestha
%A Roland Malli
%A Susanne Scheruebel
%J -
%D 2020
%R 10.1371/journal.pbio.3000700
%X Trimeric intracellular cation (TRIC) channels have been proposed to modulate Ca2+ release from the endoplasmic reticulum (ER) and determine oscillatory Ca2+ signals. Here, we report that TRIC-A¨Cmediated amplitude and frequency modulation of ryanodine receptor 2 (RyR2)-mediated Ca2+ oscillations and inositol 1,4,5-triphosphate receptor (IP3R)-induced cytosolic signals is based on attenuating store-operated Ca2+ entry (SOCE). Further, TRIC-A¨Cdependent delay in ER Ca2+ store refilling contributes to shaping the pattern of Ca2+ oscillations. Upon ER Ca2+ depletion, TRIC-A clusters with stromal interaction molecule 1 (STIM1) and Ca2+-release¨Cactivated Ca2+ channel 1 (Orai1) within ER¨Cplasma membrane (PM) junctions and impairs assembly of the STIM1/Orai1 complex, causing a decrease in Orai1-mediated Ca2+ current and SOCE. Together, our findings demonstrate that TRIC-A is a negative regulator of STIM1/Orai1 function. Thus, aberrant SOCE could contribute to muscle disorders associated with loss of TRIC-A
%K Endoplasmic reticulum
%K Fluorescence resonance energy transfer
%K Cations
%K Yellow fluorescent protein
%K Intracellular receptors
%K Kidneys
%K Protein interactions
%K Skeletal muscles
%U https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3000700