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Biologists map rare case of fitness-reducing interaction in nuclear, mitochondrial DNA
Date:2/5/2013

an assistant professor in the IU College of Arts and Sciences' Department of Biology. "This has limited our understanding of which genes harbor variants causing mitochondrial-nuclear disruption and the processes that are impacted by the co-evolution of these genomes."

Using genetic techniques and many resources available from IU's own Bloomington Drosophila Stock Center, the scientists mapped an interaction between a single mutation in a mitochondrial tRNA gene, mt-tRNA-Tyr, and an amino acid change in its nuclear-encoded charging enzyme, the mitochondrially targeted amino acyl tRNA synthetase, mt-TyrRS -- the enzyme that places the proper amino acid on the tRNA to allow for mitochondrial protein synthesis.

"As a result, the incompatibility decreases the activity of the oxidative phosphorylation pathway," Montooth said, "demonstrating that decreased mitochondrial protein synthesis compromises the energetic function required for proper development of adult structures, such as the ovary and sensory bristles."

These types of fitness-reducing genetic incompatibilities are one hypothesized mechanism that can maintain the formation of new species.


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Contact: Steve Chaplin
stjchap@iu.edu
812-856-1896
Indiana University
Source:Eurekalert  

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