Adenylate kinase 1 gene deletion disrupts muscle energetic economy despite metabolic rearrangement

EMBO J. 2000 Dec 1;19(23):6371-81. doi: 10.1093/emboj/19.23.6371.

Abstract

Efficient cellular energy homeostasis is a critical determinant of muscle performance, providing evolutionary advantages responsible for species survival. Phosphotransfer reactions, which couple ATP production and utilization, are thought to play a central role in this process. Here, we provide evidence that genetic disruption of AK1-catalyzed ss-phosphoryl transfer in mice decreases the potential of myofibers to sustain nucleotide ratios despite up-regulation of high-energy phosphoryl flux through glycolytic, guanylate and creatine kinase phosphotransfer pathways. A maintained contractile performance of AK1-deficient muscles was associated with higher ATP turnover rate and larger amounts of ATP consumed per contraction. Metabolic stress further aggravated the energetic cost in AK1(-/-) muscles. Thus, AK1-catalyzed phosphotransfer is essential in the maintenance of cellular energetic economy, enabling skeletal muscle to perform at the lowest metabolic cost.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adenine / metabolism
  • Adenosine Triphosphate / biosynthesis
  • Adenylate Kinase / chemistry
  • Adenylate Kinase / genetics*
  • Adenylate Kinase / physiology
  • Animals
  • Blotting, Northern
  • Catalysis
  • Cloning, Molecular
  • Creatine Kinase / metabolism
  • Embryo, Mammalian / metabolism
  • Gene Deletion*
  • Glucose-6-Phosphate / metabolism
  • Guanosine Diphosphate / metabolism
  • Guanosine Triphosphate / metabolism
  • Guanylate Kinases
  • Hydrogen-Ion Concentration
  • Hypoxia
  • Isoenzymes / chemistry
  • Isoenzymes / genetics*
  • Isoenzymes / physiology
  • Magnetic Resonance Spectroscopy
  • Mice
  • Mice, Knockout
  • Mice, Mutant Strains
  • Muscle, Skeletal / metabolism
  • Muscle, Skeletal / physiology*
  • Nucleoside-Phosphate Kinase / metabolism
  • Phosphotransferases / metabolism
  • Potassium Chloride / pharmacology
  • Protein Isoforms
  • Stem Cells / metabolism
  • Stress, Physiological
  • Time Factors
  • Up-Regulation

Substances

  • Isoenzymes
  • Protein Isoforms
  • Guanosine Diphosphate
  • Glucose-6-Phosphate
  • Potassium Chloride
  • Guanosine Triphosphate
  • Adenosine Triphosphate
  • Phosphotransferases
  • Creatine Kinase
  • Adenylate Kinase
  • adenylate kinase 1
  • Nucleoside-Phosphate Kinase
  • Guanylate Kinases
  • Adenine