Use of gene targeting for compromising energy homeostasis in neuro-muscular tissues: The role of sarcomeric mitochondrial creatine kinase

Karen Steeghs, Arend Heerschap, Arnold De Haan, Wim Ruitenbeek, Frank Oerlemans, Jan Van Deursen, Benjamin Perryman, Dirk Pette, Marloes Brückwilder, Jolande Koudijs, Jap Paul, Bé Wieringa

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

We have introduced a single knock-out mutation in the mitochondrial creatine kinase gene (ScCKmit) in the mouse germ line via targeted mutagenesis in mouse embryonic stem (ES) cells. Surprisingly, ScCKmit -/- muscles, unlike muscles of mice with a deficiency of cytosolic M-type creatine kinase (M-CK -/-; Van Deursen et al. (1993) Cell 74, 621-631), display no altered morphology, performance or oxidative phosphorylation capacity. Also, the levels of high energy phosphate metabolites were essentially unaltered in ScCKmit mutants. Our results challenge some of the present concepts about the strict coupling between CKmit function and aerobic respiration.

Original languageEnglish (US)
Pages (from-to)29-41
Number of pages13
JournalJournal of Neuroscience Methods
Volume71
Issue number1
DOIs
StatePublished - Jan 1997

Keywords

  • creatine kinase
  • energy homeostasis
  • gene targeting
  • mitochondria
  • muscle physiology
  • oxidative phosphorylation

ASJC Scopus subject areas

  • Neuroscience(all)

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