When Francisca Diaz, Ph.D., research assistant professor of neurology, and Carlos T. Moraes, Ph.D., professor of neurology and cell biology, developed a genetically modified mouse with a defective enzyme (cytochrome oxidase) responsible for energy production inside cells, their main interest was to study human diseases in which this enzyme is defective. This mouse has now proven useful in a study of glial cells published in the April 29 issue of the journal Nature.
Because cytochrome oxidase deficiencies are devastating and often fatal infantile genetic disorders, Diaz and Moraes used this mouse model in a number of published studies to understand and treat these diseases. However, they predicted that this mouse model could also help address several important basic biological questions. This proved to be true in several occasions, including in this recent collaboration, “Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity,” with Klaus Armin-Nave, Ph.D., professor of molecular biology and director at the Max Planck Institute for Experimental Medicine in Göttingen, Germany.
Glial cells are supportive cells in the nervous system, surrounding neurons and providing insulation between them. The team used the genetically modified mouse to show that a subgroup of glial cells, called mature oligodendrocytes, do not depend on cytochrome oxidase for survival. In addition, they showed that the oligodendrocytes can continue to provide fuel for neighboring neurons in the spinal cord even when the enzyme is non-functional.
Moraes says, “This finding on the metabolic control between cells in the spinal cord has import
University of Miami