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Researchers at UT Southwestern discover new function for old enzyme

ly have metabolic functions, and that aconitase, one of these proteins, is essential for mitochondrial DNA maintenance and inheritance, a new function independent of its normal enzyme activity."

To determine the region of aconitase that keeps mitochondrial DNA intact, Dr. Butow's group made mutations in parts of the enzyme that are important for its catalytic activity. In spite of these mutations, aconitase still functions in the maintenance of mitochondrial DNA. The researchers concluded that aconitase's role in protecting the mitochondrial genome is independent of its role in making energy, giving a new face to the long-known enzyme.

Genes in the cell's nucleus code for aconitase, and once made, the protein is shuttled to the mitochondria to serve its functions. According to Dr. Butow, aconitase may participate in an internal cell communication system known as retrograde signaling.

Retrograde signaling serves as a status-check in cells, where the mitochondria signal to the nucleus if something is wrong and when things are better again. By protecting the mitochondrial DNA, aconitase may be part of the "A-OK" signal after the cell experiences stress.

The role of aconitase in stabilizing the mitochondrial genome may be an evolutionary adaptation where the mitochondria co-opts a nuclearly encoded protein to ensure survival of its genome, said Dr. Butow. "The cell takes care of the nucleus, because that is where its genome is," he said, "but the mitochondrial genome is not looked after. It has to take care of itself."

Other UT Southwestern researchers who participated in the study are lead author Dr. Xin Jie Chen, assistant professor of molecular biology, and Xiaowen Wang, research assistant in molecular biology. Dr. Brett A. Kaufmann, a former graduate student at UT Southwestern now with the Montreal Neurological Institute, also contributed.


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Contact: Megha Satyanarayana
megha.saty@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center
3-Feb-2005


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