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First published online March 5, 2008

Journal of Cell Science 121, 605e (2008)
© The Company of Biologists Limited
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In this issue

Reversal of SOCE fortune


Figure 1

Depletion of intracellular Ca2+ stores leads to the activation of Ca2+-permeable channels in the plasma membrane, a reversible process known as store-operated Ca2+ entry (SOCE). The Ca2+ that enters through the store-operated channels can then be pumped into stores within the ER to replenish them. Depleted Ca2+ stores in the ER stimulate the ER Ca2+ sensor Stim1 to rearrange from tubular structures throughout the ER to punctate structures near the plasma membrane, where it activates the SOCE channels. On page 762, James W. Putney, Jr and colleagues investigate the poorly understood mechanism and determinants of the localisation and reversal of Stim1 puncta formation. They show that SOCE is tightly coupled to the formation of Stim1 puncta, because the basis for SOCE termination is the reversal of punctate Stim1 localisation, which, in turn, is dependent on SOCE-dependent store refilling. In addition, they report on the role of the pharmacologic agent ML-9 as a potential antagonist of Stim1-dependent SOCE. These findings provide a molecular basis for the self-regulating nature of the SOCE process.


Related articles in JCS:

Ca2+-store-dependent and -independent reversal of Stim1 localization and function
Jeremy T. Smyth, Wayne I. DeHaven, Gary S. Bird, and James W. Putney, Jr
JCS 2008 121: 762-772. [Abstract] [Full Text]  




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