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First published online 10 July 2006
doi: 10.1242/dev.02479

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The calcineurin pathway links hyperpolarization (Kir2.1)-induced Ca²⁺ signals to human myoblast differentiation and fusion

¹ Department of Clinical Neurosciences, University Hospital, Geneva, Switzerland.
² Department of Basic Neurosciences, University Medical Center, Rue Michel Servet 1, 1211 Geneva 4, Switzerland.

^* Author for correspondence (e-mail: stephane.konig{at}medecine.unige.ch)

Accepted 6 June 2006

In human myoblasts triggered to differentiate, a hyperpolarization, resulting from K⁺ channel (Kir2.1) activation, allows the generation of an intracellular Ca²⁺ signal. This signal induces an increase in expression/activity of two key transcription factors of the differentiation process, myogenin and MEF2. Blocking hyperpolarization inhibits myoblast differentiation. The link between hyperpolarization-induced Ca²⁺ signals and the four main regulatory pathways involved in myoblast differentiation was the object of this study. Of the calcineurin, p38-MAPK, PI3K and CaMK pathways, only the calcineurin pathway was inhibited when Kir2.1-linked hyperpolarization was blocked. The CaMK pathway, although Ca²⁺ dependent, is unaffected by changes in membrane potential or block of Kir2.1 channels. Concerning the p38-MAPK and PI3K pathways, their activity is present already in proliferating myoblasts and they are unaffected by hyperpolarization or Kir2.1 channel block. We conclude that the Kir2.1-induced hyperpolarization triggers human myoblast differentiation via the activation of the calcineurin pathway, which, in turn, induces expression/activity of myogenin and MEF2.

Key words: Myogenesis, Calcineurin, Hyperpolarization, Human myoblasts

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