TRIC-A shapes oscillatory Ca2+ signals by interaction with STIM1/Orai1 complexes.

Autor: Niroj Shrestha, Bernadett Bacsa, Hwei Ling Ong, Susanne Scheruebel, Helmut Bischof, Roland Malli, Indu Suresh Ambudkar, Klaus Groschner
Jazyk: angličtina
Rok vydání: 2020
Předmět:
Zdroj: PLoS Biology, Vol 18, Iss 4, p e3000700 (2020)
Druh dokumentu: article
ISSN: 1544-9173
1545-7885
DOI: 10.1371/journal.pbio.3000700
Popis: 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-mediated 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-dependent 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-activated Ca2+ channel 1 (Orai1) within ER-plasma 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.
Databáze: Directory of Open Access Journals
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