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Published 14 March 2005. doi:10.1083/jcb.200408128
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 168, Number 6, 887-897
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Article

 Activity-dependent and -independent nuclear fluxes of HDAC4 mediated by different kinases in adult skeletal muscle

Yewei Liu1, William R. Randall2, and Martin F. Schneider1

1 Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, MD 21201
2 Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore, MD 21201

Correspondence to M.F. Schneider: mschneid{at}umaryland.edu

Class II histone deacetylases (HDACs) may decrease slow muscle fiber gene expression by repressing myogenic transcription factor myocyte enhancer factor 2 (MEF2). Here, we show that repetitive slow fiber type electrical stimulation, but not fast fiber type stimulation, caused HDAC4-GFP, but not HDAC5-GFP, to translocate from the nucleus to the cytoplasm in cultured adult skeletal muscle fibers. HDAC4-GFP translocation was blocked by calmodulin-dependent protein kinase (CaMK) inhibitor KN-62. Slow fiber type stimulation increased MEF2 transcriptional activity, nuclear Ca2+ concentration, and nuclear levels of activated CaMKII, but not total nuclear CaMKII or CaM-YFP. Thus, calcium transients for slow, but not fast, fiber stimulation patterns appear to provide sufficient Ca2+-dependent activation of nuclear CaMKII to result in net nuclear efflux of HDAC4. Nucleocytoplasmic shuttling of HDAC4-GFP in unstimulated resting fibers was not altered by KN-62, but was blocked by staurosporine, indicating that different kinases underlie nuclear efflux of HDAC4 in resting and stimulated muscle fibers.

Abbreviations used in this paper: AOI, areas of interest; CaMK, calmodulin-dependent protein kinase; CsA, cyclosporin A; FDB, flexor digitorum brevis; HDAC, histone deacetylase; MEF2, myocyte enhancer factor 2; NFAT, nuclear factor of activated T cells.


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