Abstract
The elusive coupling between endoplasmic reticulum (ER) Ca2+ stores and plasma membrane (PM) 'storeoperated' Ca2+ entry channels was probed through a novel combination of cytoskeletal modifications. Whereas coupling was unaffected by disassembly of the actin cytoskeleton, in situ redistribution of F-actin into a tight cortical layer subjacent to the PM displaced cortical ER and prevented coupling between ER and PM Ca2+ entry channels, while not affecting inositol 1,4,5-trisphosphate-mediated store release. Importantly, disassembly of the induced cortical actin layer allowed ER to regain access to the PM and reestablish coupling of Ca2+ entry channels to Ca2+ store depletion. Coupling is concluded to be mediated by a physical 'secretion-like' mechanism involving close but reversible interactions between the ER and the PM.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 487-499 |
| Number of pages | 13 |
| Journal | Cell |
| Volume | 98 |
| Issue number | 4 |
| DOIs | |
| State | Published - Aug 20 1999 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
Cite this
Store-operated Ca2+ entry : Evidence for a secretion-like coupling model. / Patterson, R. L.; Van Rossum, D. B.; Gill, D. L.
In: Cell, Vol. 98, No. 4, 20.08.1999, p. 487-499.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Store-operated Ca2+ entry
T2 - Evidence for a secretion-like coupling model
AU - Patterson, R. L.
AU - Van Rossum, D. B.
AU - Gill, D. L.
PY - 1999/8/20
Y1 - 1999/8/20
N2 - The elusive coupling between endoplasmic reticulum (ER) Ca2+ stores and plasma membrane (PM) 'storeoperated' Ca2+ entry channels was probed through a novel combination of cytoskeletal modifications. Whereas coupling was unaffected by disassembly of the actin cytoskeleton, in situ redistribution of F-actin into a tight cortical layer subjacent to the PM displaced cortical ER and prevented coupling between ER and PM Ca2+ entry channels, while not affecting inositol 1,4,5-trisphosphate-mediated store release. Importantly, disassembly of the induced cortical actin layer allowed ER to regain access to the PM and reestablish coupling of Ca2+ entry channels to Ca2+ store depletion. Coupling is concluded to be mediated by a physical 'secretion-like' mechanism involving close but reversible interactions between the ER and the PM.
AB - The elusive coupling between endoplasmic reticulum (ER) Ca2+ stores and plasma membrane (PM) 'storeoperated' Ca2+ entry channels was probed through a novel combination of cytoskeletal modifications. Whereas coupling was unaffected by disassembly of the actin cytoskeleton, in situ redistribution of F-actin into a tight cortical layer subjacent to the PM displaced cortical ER and prevented coupling between ER and PM Ca2+ entry channels, while not affecting inositol 1,4,5-trisphosphate-mediated store release. Importantly, disassembly of the induced cortical actin layer allowed ER to regain access to the PM and reestablish coupling of Ca2+ entry channels to Ca2+ store depletion. Coupling is concluded to be mediated by a physical 'secretion-like' mechanism involving close but reversible interactions between the ER and the PM.
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U2 - 10.1016/S0092-8674(00)81977-7
DO - 10.1016/S0092-8674(00)81977-7
M3 - Article
VL - 98
SP - 487
EP - 499
JO - Cell
JF - Cell
SN - 0092-8674
IS - 4
ER -