Alfonzo noted that the current study was able to determine that the import of tRNAs occurs, but it leaves open the question of how it happens.
He and colleagues conducted experiments first in rat liver cells to test whether tRNA import occurs in mammals at all. When the import was observed in rat mitochondria, they extended the study to human cells.
The finding that tRNA import occurs in humans can set in motion an entirely new line of research into therapeutic options for patients with diseases caused by mitochondrial defects. There appears to be no way to introduce healthy tRNAs directly into mitochondria because their membranes have proven impenetrable to such outside interference, Alfonzo explained.
So scientists know they would have to rely on the import process that starts in the cytoplasm to transfer healthy tRNAs to damaged mitochondria and improve energy production.
Until now, researchers didn't know the human mitochondria had that import ability, so scientists were going to try using protozoan or yeast cells to manipulate the import process in human cells.
"What we are saying is you don't need to bring up new machinery from a different organism because human cells already come equipped with their own way to import tRNAs. There is no need to cross species," Alfonzo said. "What we need to know now is what proteins are involved in the import mechanism so we can exploit the process for therapy."
One compound already identified as essential for the process is Adenosine-5-triphosphate, or ATP, a compound associated with energy transport in cells. Alfonzo and colleagues demonstrated ATP's role in the process using cells from a patient with a specific type of epilepsy called MERRF. This disease is characterized by a mitochondrial tRNA mutation leading to a drastic reduction in the mitochondria's ability to generate ATP, which in turn hinders the import of tRNAs into the mitochondria of people wit
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| Contact: Juan Alfonzo Alfonzo.1@osu.edu 614-292-0004 Ohio State University Source:Eurekalert |