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Ca2+ tunneling architecture and function are important for secretion
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DOI：10.1083/jcb.202402107.png)
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摘要
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Ca2+ tunneling requires both store-operated Ca2+ entry (SOCE) and Ca2+ release from the endoplasmic reticulum (ER). Tunneling expands the SOCE microdomain through Ca2+ uptake by SERCA into the ER lumen where it diffuses and is released via IP3 receptors. In this study, using high-resolution imaging, we outline the spatial remodeling of the tunneling machinery (IP3R1; SERCA; PMCA; and Ano1 as an effector) relative to STIM1 in response to store depletion. We show that these modulators redistribute to distinct subdomains laterally at the plasma membrane (PM) and axially within the cortical ER. To functionally define the role of Ca2+ tunneling, we engineered a Ca2+ tunneling attenuator (CaTAr) that blocks tunneling without affecting Ca2+ release or SOCE. CaTAr inhibits Cl- secretion in sweat gland cells and reduces sweating in vivo in mice, showing that Ca2+ tunneling is important physiologically. Collectively our findings argue that Ca2+ tunneling is a fundamental Ca2+ signaling modality.
Keyword:
ENDOPLASMIC-RETICULUM
CRAC CHANNELS
ER LUMEN
ENTRY
STIM1
ORAI1
RELEASE
ION
VISUALIZATION
DIFFUSION
期刊
IF:
6.4
论文数:
1.2W
被引数:
5.7W
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引用论文
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A STIM1-dependent 'trafficking trap' mechanism regulates Orai1 plasma membrane residence and Ca2+ influx levelsSTIM1-dependent的 “贩运陷阱” 机制调节Orai1质膜居住和Ca2流入水平
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