John E. Wilson
Emeritus Professor

• B.S. 1961, University of Notre Dame
• M.S. 1962, University of Notre Dame
• Ph.D. 1964, University of Illinois
• Postdoctoral Associate, 1964-65, University of Illinois
• Research Biochemist, 1965-67, U.S. Army Medical Research Laboratory, Edgewood Arsenal, Maryland
• Visiting Professor, 1974, Medical Research Council Laboratory, Carshalton, England
• Visiting Professor, 1981, Griffith University, Brisbane, Australia
• MSU Distinguished Faculty Award, 1991

wilsonj@msu.edu
Department of Biochemistry
Michigan State University
East Lansing, MI 48824-1319

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John E. Wilson

Research Interests

Glucose is, under normal conditions, virtually the sole substrate supporting the intense energy metabolism required for brain function. Hexokinase catalyzes the initial step in metabolism of glucose, and regulation of hexokinase activity is generally recognized as a major factor governing the rate of cerebral glucose metabolism. How hexokinase is regulated, with activity increased during periods of increased neurophysiological activity and decreased when energy demands subside, is the focus of our research. This regulation is complex. Classical allosteric inhibition by the product, glucose 6-phosphate, is undoubtedly a factor. However, hexokinase binds to the outer mitochondrial membrane and there is clear evidence that this physical association leads to close metabolic interactions with intramitochondrial oxidative phosphorylation, and that this is also of regulatory significance.

We are interested in the molecular basis for interaction of hexokinase with mitochondria, and for the resultant close coupling of glucose phosphorylating activity with intramitochondrial ATP production. The levels of hexokinase vary markedly in different brain regions, and are generally correlated with basal levels of glucose utilization. Chronic perturbations of neurophysiological function result in altered rates of glucose utilization and hexokinase activity in the affected region. There is reason to believe that this is, at least partly, due to regulation at the transcriptional level, and hence we are involved in characterization of the elements regulating the transcription of this gene. While our major focus is on the Type I isozyme of hexokinase, the predominant form in brain, we have a general interest in the structure and function of other mammalian hexokinases, particularly the Type II and Type III isozymes. We are interested in the comparative enzymology of the hexokinase isozymes, and in defining their unique roles in cellular metabolism. All of this requires a synthesis of information gained from studies employing techniques of enzymology, molecular biology, membrane biochemistry, and neurochemistry.

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