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First published online April 5, 2006

Journal of Cell Science 119, 801e (2006)
© The Company of Biologists Limited
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In this issue

NFAT sets the pace


Figure 1

Skeletal muscles contain slow, fatigue-resistant fibres that depend on oxidative phosphorylation for energy and fast glycolytic fibres, which tire quickly. Individual muscle fibres can adapt, however, to changing functional demands. On p. 1604, Stefano Schiaffino and co-workers demonstrate that nerve activity can control fibre type in vivo by regulating nucleocytoplasmic shuttling of the transcription factor NFATc1. NFATc1 activity is controlled by Ca2+-calcineurin signalling – calcineurin dephosphorylates NFATc1, which translocates to the nucleus and induces a gene expression program typical of slow oxidative muscle fibres. By transfecting fast (tibialis anterior) and slow (soleus) mouse muscles with a plasmid encoding NFATc1-GFP, Schiaffino's team show that NFATc1 is predominantly cytoplasmic in fast muscle but nuclear in slow muscle. Furthermore, they report, enforced inactivity causes nuclear export of NFATc1 in slow muscle, whereas electrostimulation of fast muscle to mimic the firing of slow motor neurons causes rapid nuclear import of NFATc1. These and other results lead the authors to conclude that NFATc1 is a nerve `activity sensor' in skeletal muscle fibres in vivo.


Related articles in JCS:

NFATc1 nucleocytoplasmic shuttling is controlled by nerve activity in skeletal muscle
Jana Tothova, Bert Blaauw, Giorgia Pallafacchina, Rüdiger Rudolf, Carla Argentini, Carlo Reggiani, and Stefano Schiaffino
JCS 2006 119: 1604-1611. [Abstract] [Full Text]  




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