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Published 17 September 2001. doi:10.1083/jcb.200106156
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© The Rockefeller University Press, 0021-9525/2001/9/1225 $5.00
The Journal of Cell Biology, Volume 154, Number 6, September 17, 2001 1225-1234

Article

Essential control of an endothelial cell ISOC by the spectrin membrane skeleton



Songwei Wu1, Jose Sangerman2, Ming Li1, George H. Brough1, Steven R. Goodman3 and Troy Stevens1

1 Department of Pharmacology, College of Medicine, University of South Alabama, Mobile, AL 36688
2 Department of Cell Biology and Neuroscience, College of Medicine, University of South Alabama, Mobile, AL 36688
3 Department of Molecular and Cell Biology, University of Texas, Dallas, TX 75083

Address correspondence to Troy Stevens, Department of Pharmacology, MSB 3360, University of South Alabama College of Medicine, Mobile, AL 36688. Tel.: (334) 460-6010. Fax: (334) 460-6798. E-mail:tstevens{at}jaguar1.usouthal.edu

Mechanism(s) underlying activation of store-operated Ca2+ entry currents, ISOC, remain incompletely understood. F-actin configuration is an important determinant of channel function, although the nature of interaction between the cytoskeleton and ISOC channels is unknown. We examined whether the spectrin membrane skeleton couples Ca2+ store depletion to Ca2+ entry. Thapsigargin activated an endothelial cell ISOC (-45 pA at -80 mV) that reversed at +40 mV, was inwardly rectifying when Ca2+ was the charge carrier, and was inhibited by La3+ (50 µM). Disruption of the spectrin–protein 4.1 interaction at residues A207-V445 of ßSpII{Sigma}1 decreased the thapsigargin-induced global cytosolic Ca2+ response by 50% and selectively abolished the endothelial cell ISOC, without altering activation of a nonselective current through cyclic nucleotide–gated channels. In contrast, disruption of the spectrin–actin interaction at residues A47-K186 of ßSpII{Sigma}1 did not decrease the thapsigargin-induced global cytosolic Ca2+ response or inhibit ISOC. Results indicate that the spectrin–protein 4.1 interaction selectively controls ISOC, indicating that physical coupling between calcium release and calcium entry is reliant upon the spectrin membrane skeleton.

Key Words: store-operated Ca2+ entry; capacitative Ca2+ entry; ICRAC; protein 4.1; F-actin


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