Rather than moving to the ends of the cells, or synapses, where cell-to-cell communication takes place, mitochondria in mutant fruit flies just piled up in the center of the cell. Even so, the mutant cells could still transmit signals, although not as well.

The findings are surprising because scientists had thought any disruption in normal mitochondrial behavior would be lethal in the embryo stage. Instead, the mutant fruit fly larvae survive for five days, although they don't live to adulthood.

"Everyone believed that mitochondria are essential at synapses -- and this is wrong," said research team leader Konrad E. Zinsmaier, a University of Arizona associate professor of neurobiology at the Arizona Research Laboratories' Division of Neurobiology. "The mutation allows us to study what mitochondria are really good for." The finding provides scientists with additional insight into how nerve cells work and provides a basis for understanding how such dysfunctions cause neurodegenerative diseases.

The researchers will publish their findings in the August 4 issue of the journal Neuron. A complete list of authors and their affiliations can be found at the end of this release.

Little is known about what causes mitochondria to become dysfunctional and how they contribute to neurological disorders. To learn more about what could go wrong with the energy units, Zinsmaier and his colleagues induced a mutation in the fruit fly mitochondrial protein, dMiro. dMiro stands for Drosophila mitochondrial Rho-like GTPase.

Molecular motors shuttle mitochondria within cells along cellular highways called microtubules. Normally, the mitochondria travel the le
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Contact: Mari N. Jensen
mnjensen@email.arizona.edu
520-626-9635
University of Arizona
3-Aug-2005