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Skeletal muscle CaMKII enriches in nuclei and phosphorylates myogenic factor SRF at multiple sites

M Flück1, F W Booth, M N Waxham

  • 1Department of Integrative Biology and Pharmacology, University of Texas Medical School, Houston, Texas 77030, USA. flueck@mem.unibe.ch

Insights

Calcium/calmodulin-dependent protein kinase II (CaMKII) phosphorylates the myogenic factor SRF at multiple sites, including novel Thr-160 in its MADS box. This phosphorylation by nuclear CaMKII may regulate SRF

Area of Science:

  • Molecular biology
  • Cell signaling
  • Muscle physiology

Background:

  • Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) plays crucial roles in cellular signaling.
  • SRF is a key myogenic factor regulating muscle gene expression.
  • Understanding CaMKII's role in skeletal muscle is vital for muscle development and function.

Purpose of the Study:

  • To characterize CaMKII activity in skeletal muscle.
  • To investigate the phosphorylation of SRF by CaMKII.
  • To identify specific phosphorylation sites on SRF.

Main Methods:

  • Skeletal muscle homogenates and nuclear extracts were used.
  • In vitro phosphorylation assays with recombinant CaMKII and SRF.
  • SDS-PAGE and phosphopeptide mapping.
  • Microsequencing of phosphorylated peptides.

Main Results:

  • CaMKII isoforms from skeletal muscle efficiently phosphorylated SRF in vitro.
  • Multiple phosphorylation sites were identified on SRF within amino acids 1-171.
  • Ser-103 and a novel site, Thr-160 in the MADS box, were identified as phosphorylation sites.
  • CaMKII activity was enriched in nuclear extracts, phosphorylating nuclear SRF.

Conclusions:

  • CaMKII phosphorylates SRF at multiple sites, including Thr-160 in the MADS box.
  • Nuclear CaMKII activity targets SRF for phosphorylation.
  • Phosphorylation of Thr-160 may directly impact SRF DNA binding and function.

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