Constitutive recycling of the store-operated Ca<sup>2+</sup>channel Orai1 and its internalization during meiosis

Yu, F. Richard; Sun, Lu; Machaca, Khaled

doi:10.1085/jgp1366oia6

Cited by 20 publications

(30 citation statements)

References 22 publications

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“…In flies expressing the dominant negative form of Rab5, TRPL remains in the rhabdomeres and does not translocate to the cell body upon illumination [46]. It has been reported that Rab5 co-localizes with Orai1 in oocytes and eggs and mediates Orai1 internalization during meiosis in oocytes [47]. However, we did not detect any effect of Rab5 on Orai1-STIM1 function.…”

Section: Accepted Manuscriptcontrasting

confidence: 80%

Fast endocytic recycling determines TRPC1–STIM1 clustering in ER–PM junctions and plasma membrane function of the channel

Souza

Ong

Liu

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Stromal interaction molecule 1 (STIM1) senses depletion of ER-Ca2+ store and clusters in ER-PM junctions where it associates with and gates Ca2+ influx channels, Orai1 and TRPC1. Clustering of TRPC1 with STIM1 and Orai1 in these junctions is critical since Orai1-mediated Ca2+ entry triggers surface expression of TRPC1 while STIM1 gates the channel. Thus, plasma membrane function of TRPC1 depends on the delivery of the channel to the sites where STIM1 puncta are formed. This study examines intracellular trafficking mechanism(s) that determine plasma membrane expression and function of TRPC1 in cells where Orai1 and TRPC1 are endogenously expressed and contribute to Ca2+ entry. We report that TRPC1 is internalized by Arf6-dependent pathway, sorted to Rab5-containing early endosomes, and trafficked to ER-PM junctions by Rab4-dependent fast recycling. Overexpression of Arf6, or Rab5, but not the respective dominant negative mutants, induced retention of TRPC1 in early endosomes and suppressed TRPC1 function. Notably, cells expressing Arf6 or Rab5 displayed an inwardly rectifying ICRAC current that is mediated by Orai1 instead of TRPC1-associated ISOC, demonstrating that Orai1 function was not altered. Importantly, expression of Rab4, but not STIM1, with Rab5 rescued surface expression and function of TRPC1, restoring generation of ISOC. Together, these data demonstrate that trafficking via fast recycling endosomes determines TRPC1-STIM1 clustering within ER-PM junctions following ER-Ca2+ store depletion which is critical for the surface expression and function of the channel. Ca2+ influx mediated by TRPC1 modifies Ca2+-dependent physiological response of cells.

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Section: Accepted Manuscriptcontrasting

confidence: 80%

Fast endocytic recycling determines TRPC1–STIM1 clustering in ER–PM junctions and plasma membrane function of the channel

Souza

Ong

Liu

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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“…Although speculative at this point, SOCE inactivation may prevent maverick Ca 2+ signals during cellular division that may interfere with normal cell division especially given the potential role of Ca 2+ signals during M-phase as discussed in details above [136]. SOCE inactivation was recently shown to be due to both internalization of the Orai1 channel and the inability of STIM1 to form clusters in response to store depletion in oocytes [137;138]. …”

Section: Introductionmentioning

confidence: 99%

Ca2+ signaling, genes and the cell cycle

Machaca

2010

Cell Calcium

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Changes in the concentration and spatial distribution of Ca2+ ions in the cytoplasm constitute a ubiquitous intracellular signaling module in cellular physiology. With the advent of Ca2+ dyes that allow direct visualization of Ca2+ transients, combined with powerful experimental tools such as electrophysiological recordings, intracellular Ca2+ transients have been implicated in practically every aspect of cellular physiology, including cellular proliferation. Ca2+ signals are associated with different phases of the cell cycle and interfering with Ca2+ signaling or downstream pathways often disrupts progression of the cell cycle. Although there exists a dependence between Ca2+ signals and the cell cycle the mechanisms involved are not well defined and given the cross-talk between Ca2+ and other signaling modules, it is difficult to assess the exact role of Ca2+ signals in cell cycle progression. Two exceptions however, include fertilization and T-cell activation, where well-defined roles for Ca2+ signals in mediating progression through specific stages of the cell cycle have been clearly established. In the case of T-cell activation Ca2+ regulates entry into the cell cycle through the induction of gene transcription.

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“…Recently, it has been shown that most Orai1 is situated in an endosomal compartment under resting conditions, and that it cycles continuously between this compartment and the PM through SNAP‐25‐dependent exocytosis (41, 42). To examine the role of Orai1 exocytosis we examined CFTR regulation of calcium entry in the presence of N ‐ethylmaleimide (NEM), an inhibitor of SNARE proteins.…”

Section: Resultsmentioning

confidence: 99%

Enhanced Ca²⁺entry due to Orai1 plasma membrane insertion increases IL‐8 secretion by cystic fibrosis airways

Balghi¹,

Robert²,

Rappaz³

et al. 2011

FASEB j.

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Cystic fibrosis (CF) is caused by mutations in the gene encoding the CF transmembrane conductance regulator (CFTR). The most common mutation, ΔF508, causes retention of CFTR in the endoplasmic reticulum (ER). Some CF abnormalities can be explained by altered Ca(2+) homeostasis, although it remains unknown how CFTR influences calcium signaling. This study examined the novel hypothesis that store-operated calcium entry (SOCE) through Orai1 is abnormal in CF. The significance of Orai1-mediated SOCE for increased interleukin-8 (IL-8) expression in CF was also investigated. CF and non-CF human airway epithelial cell line and primary cells (obtained at lung transplantation) were used in Ca(2+) imaging, electrophysiology, and fluorescence imaging experiments to explore differences in Orai1 function in CF vs. non-CF cells. Protein expression and localization was assessed by Western blots, cell surface biotinylation, ELISA, and image correlation spectroscopy (ICS). We show here that store-operated Ca(2+) entry (SOCE) is elevated in CF human airway epithelial cells (hAECs; ≈ 1.8- and ≈ 2.5-fold for total Ca(2+)(i) increase and Ca(2+) influx rate, respectively, and ≈ 2-fold increase in the I(CRAC) current) and is caused by increased exocytotic insertion (≈ 2-fold) of Orai1 channels into the plasma membrane, which is normalized by rescue of ΔF508-CFTR trafficking to the cell surface. Augmented SOCE in CF cells is a major factor leading to increased IL-8 secretion (≈ 2-fold). CFTR normally down-regulates the Orai1/stromal interaction molecule 1 (STIM1) complex, and loss of this inhibition due to the absence of CFTR at the plasma membrane helps to explain the potentiated inflammatory response in CF cells.

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Constitutive recycling of the store-operated Ca²⁺channel Orai1 and its internalization during meiosis

Abstract: Abbreviations used in this paper: Cav, caveolin; CTB, cholera toxin B; GVBD, germinal vesicle breakdown; MCD, methyl--cyclodextrin; SOCE, store-operated Ca 2+ entry; STIM1, stromal interaction molecule 1.

Cited by 20 publications

References 22 publications

Fast endocytic recycling determines TRPC1–STIM1 clustering in ER–PM junctions and plasma membrane function of the channel

Fast endocytic recycling determines TRPC1–STIM1 clustering in ER–PM junctions and plasma membrane function of the channel

Ca2+ signaling, genes and the cell cycle

Enhanced Ca²⁺entry due to Orai1 plasma membrane insertion increases IL‐8 secretion by cystic fibrosis airways

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Constitutive recycling of the store-operated Ca2+channel Orai1 and its internalization during meiosis

Abstract: Abbreviations used in this paper: Cav, caveolin; CTB, cholera toxin B; GVBD, germinal vesicle breakdown; MCD, methyl--cyclodextrin; SOCE, store-operated Ca 2+ entry; STIM1, stromal interaction molecule 1.

Cited by 20 publications

References 22 publications

Fast endocytic recycling determines TRPC1–STIM1 clustering in ER–PM junctions and plasma membrane function of the channel

Fast endocytic recycling determines TRPC1–STIM1 clustering in ER–PM junctions and plasma membrane function of the channel

Ca2+ signaling, genes and the cell cycle

Enhanced Ca2+entry due to Orai1 plasma membrane insertion increases IL‐8 secretion by cystic fibrosis airways

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Constitutive recycling of the store-operated Ca²⁺channel Orai1 and its internalization during meiosis

Enhanced Ca²⁺entry due to Orai1 plasma membrane insertion increases IL‐8 secretion by cystic fibrosis airways