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Genetics Mitochondria

Researchers at UT Southwestern discover new function for old enzyme

19 years, 2 months ago

8055  0
Posted on Feb 04, 2005, 11 a.m. By Bill Freeman

In a step toward understanding the early evolution of the cell, researchers at UT Southwestern Medical Center have discovered that an enzyme important in the production of energy also protects the mitochondria, the energy factory itself. The enzyme, called aconitase, is a well-known component of the pathway in cells that produces energy.
In a step toward understanding the early evolution of the cell, researchers at UT Southwestern Medical Center have discovered that an enzyme important in the production of energy also protects the mitochondria, the energy factory itself. The enzyme, called aconitase, is a well-known component of the pathway in cells that produces energy. But in a study using baker's yeast, Dr. Ronald Butow, professor of molecular biology, has shown a new function for the enzyme &endash; keeping the mitochondrial genome intact.

The study is available online and in the Feb. 4 edition of the journal Science.

Mitochondria are the powerhouses of cells and create energy for all cellular processes. It is thought that mitochondria are descended from bacteria that originally took up residence in early cells. Through elements of a little-understood symbiotic relationship between the bacteria and the cell, the bacteria lost their independence and evolved into an organelle that provides energy for the cell. The relationship between mitochondria and the cell make each vital to the other's survival, and may explain a key biological event &endash; the development of an efficient energy producer to fuel the evolution of more complex life forms.

Because of their supposed microbial origins, mitochondria have their own DNA, which is separate from the DNA in the cell nucleus. Cells that have lost their mitochondrial DNA do not pass on working mitochondria when they divide. Without working mitochondria, cells cannot produce energy efficiently. Events that lead to mitochondrial DNA defects are associated with neuromuscular diseases and premature aging disorders in humans.

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