Ca2+ store depletion causes STIM1 to accumulate in ER regions closely associated with the plasma membrane

被引:645
作者
Wu, Minnie M. [1 ]
Buchanan, JoAnn [1 ]
Luik, Riina M. [1 ]
Lewis, Richard S. [1 ]
机构
[1] Stanford Univ, Sch Med, Dept Mol & Cellular Physiol, Stanford, CA 94305 USA
关键词
D O I
10.1083/jcb.200604014
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Stromal interacting molecule 1 (STIM1), reported to be an endoplasmic reticulum ( ER) Ca2+ sensor controlling store-operated Ca2+ entry, redistributes from a diffuse ER localization into puncta at the cell periphery after store depletion. STIM1 redistribution is proposed to be necessary for Ca2+ release-activated Ca2+ ( CRAC) channel activation, but it is unclear whether redistribution is rapid enough to play a causal role. Furthermore, the location of STIM1 puncta is uncertain, with recent reports supporting retention in the ER as well as insertion into the plasma membrane (PM). Using total internal reflection fluorescence (TIRF) microscopy and patch-clamp recording from single Jurkat cells, we show that STIM1 puncta form several seconds before CRAC channels open, supporting a causal role in channel activation. Fluorescence quenching and electron microscopy analysis reveal that puncta correspond to STIM1 accumulation in discrete subregions of junctional ER located 10-25 nm from the PM, without detectable insertion of STIM1 into the PM. Roughly one third of these ER-PM contacts form in response to store depletion. These studies identify an ER structure underlying store-operated Ca2+ entry, whose extreme proximity to the PM may enable STIM1 to interact with CRAC channels or associated proteins.
引用
收藏
页码:803 / 813
页数:11
相关论文
共 40 条
  • [1] Assembly of presynaptic active zones from cytoplasmic transport packets
    Ahmari, SE
    Buchanan, J
    Smith, SJ
    [J]. NATURE NEUROSCIENCE, 2000, 3 (05) : 445 - 451
  • [2] An examination of the secretion-like coupling model for the activation of the Ca2+ release-activated Ca2+ current ICRAC in RBL-1 cells
    Bakowski, D
    Glitsch, MD
    Parekh, AB
    [J]. JOURNAL OF PHYSIOLOGY-LONDON, 2001, 532 (01): : 55 - 71
  • [3] Endoplasmic reticulum of animal cells and its organization into structural and functional domains
    Baumann, O
    Walz, B
    [J]. INTERNATIONAL REVIEW OF CYTOLOGY - A SURVEY OF CELL BIOLOGY, VOL 205, 2001, 205 : 149 - 214
  • [4] Enhancement of calcium signalling dynamics and stability by delayed modulation of the plasma-membrane calcium-ATPase in human T cells
    Bautista, DM
    Hoth, M
    Lewis, RS
    [J]. JOURNAL OF PHYSIOLOGY-LONDON, 2002, 541 (03): : 877 - 894
  • [5] Berridge Michael, 2004, Sci STKE, V2004, ppe33
  • [6] PERTURBATION OF CELLULAR CALCIUM INDUCES SECRETION OF LUMINAL ER PROTEINS
    BOOTH, C
    KOCH, GLE
    [J]. CELL, 1989, 59 (04) : 729 - 737
  • [7] TRANSPORT INTO AND OUT OF THE GOLGI-COMPLEX STUDIED BY TRANSFECTING CELLS WITH CDNAS ENCODING HORSERADISH-PEROXIDASE
    CONNOLLY, CN
    FUTTER, CE
    GIBSON, A
    HOPKINS, CR
    CUTLER, DF
    [J]. JOURNAL OF CELL BIOLOGY, 1994, 127 (03) : 641 - 652
  • [8] Intracellular Ca2+ release triggers translocation of membrane marker FM1-43 from the extracellular leaflet of plasma membrane into endoplasmic reticulum in T lymphocytes
    Dadsetan, S
    Shishkin, V
    Fomina, AF
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (16) : 16377 - 16382
  • [9] Regulated endocytic routing modulates wingless signaling in Drosophila embryos
    Dubois, L
    Lecourtois, M
    Alexandre, C
    Hirst, E
    Vincent, JP
    [J]. CELL, 2001, 105 (05) : 613 - 624
  • [10] Calcium-pump inhibitors induce functional surface expression of ΔF508-CFTR protein in cystic fibrosis epithelial cells
    Egan, ME
    Glöckner-Pagel, J
    Ambrose, CA
    Cahill, PA
    Pappoe, L
    Balamuth, N
    Cho, E
    Canny, S
    Wagner, CA
    Geibel, J
    Caplan, MJ
    [J]. NATURE MEDICINE, 2002, 8 (05) : 485 - 492