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First published online February 8, 2006

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Skin-deep Ca²⁺ signalling from the Golgi

The differentiation, adhesion and motility of keratinocytes - as in many cells - are controlled by intracellular Ca²⁺. Most non-excitable cells release Ca²⁺ from the endoplasmic reticulum (ER) to mediate Ca²⁺ signalling, but Alain Hovnanian, Theodora Mauro and colleagues now report that keratinocytes are unique in using Ca²⁺ stored in the Golgi (see p. 671). The skin disorder Darier disease is caused by mutations in ATP2A2, which encodes the Ca²⁺ ATPase SERCA2 that sequesters Ca²⁺ in the ER. The authors describe how keratinocytes from Darier disease patients respond normally to increases in extracellular Ca²⁺ levels (which provoke intracellular Ca²⁺ release) despite impaired ER Ca²⁺ stores. This normal response results from upregulation of the Golgi Ca²⁺ ATPase hSPCA1. Furthermore, inactivation of the gene encoding hSPCA1 - ATP2C1, mutations in which cause the skin disorder Hailey-Hailey disease - diminishes the viability of Darier disease keratinocytes. The authors therefore conclude that the Golgi Ca²⁺ ATPase plays an essential role in Ca²⁺ signalling in the keratinocyte.

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Related articles in JCS:

Activity of the hSPCA1 Golgi Ca²⁺ pump is essential for Ca²⁺-mediated Ca²⁺ response and cell viability in Darier disease

Lucie Foggia, Ida Aronchik, Karin Aberg, Barbara Brown, Alain Hovnanian, and Theodora M. Mauro
JCS 2006 119: 671-679. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?