Journal
JOURNAL OF CELL BIOLOGY
Volume 202, Issue 4, Pages 699-713Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.201301016
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Funding
- Medical Research Council
- Wellcome Trust [085295]
- Portuguese Foundation for Science and Technology (Fundacao para a Ciencia e a Tecnologia)
- Royal Society University Research Fellowship
- St. John's College, Cambridge
- Medical Research Council [G0900049, G0900224] Funding Source: researchfish
- MRC [G0900224, G0900049] Funding Source: UKRI
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Golgi antiapoptotic proteins (GAAPs) are highly conserved Golgi membrane proteins that inhibit apoptosis and promote Ca2+ release from intracellular stores. Given the role of Ca2+ in controlling cell adhesion and motility, we hypothesized that human GAAP (hGAAP) might influence these events. In this paper, we present evidence that hGAAP increased cell adhesion, spreading, and migration in a manner that depended on the C-terminal domain of hGAAP. We show that hGAAP increased store-operated Ca2+ entry and thereby the activity of calpain at newly forming protrusions. These hGAAP-dependent effects regulated focal adhesion dynamics and cell migration. Indeed, inhibition or knockdown of calpain 2 abrogated the effects of hGAAP on cell spreading and migration. Our data reveal that hGAAP is a novel regulator of focal adhesion dynamics, cell adhesion, and migration by controlling localized Ca2+-dependent activation of calpain.
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