"We found that putting these cells under stress similar to that initially encountered by the trypanosome inside the fly caused the parasites to cleave free GPIs," said Mensa-Wilmot, "and that gives us important information about how the trypanosome cell functions."
The new tools aren't just helpful in understanding GPIs in T. brucei, either. The team found that it works just as well in understanding the parasite Leishmania, which causes another pervasive and terrible tropical disease called Leishmaniasis. This debilitating disease is found is more than 88 countries where a third of a billion people are at risk to contract it.
In the same set of experiments, the researchers discovered a new pathway for protein movement in the trypanosome that may also be found in other cell types including humans. The scientists discovered that proteins can move from a glycosome, an important energy-generating organelle in a trypanosome, to the endoplasmic reticulum where GPIs are made, in response to cell stress.
The human equivalent of a glycosome is a peroxisome, whose malfunction is associated with diseases such as Zellweger Syndrome. According to the National Institute of Neurological Disorders and Stroke, symptoms of this disorder at birth "may include lack of muscle tone and an inability to move. Other symptoms may include unusual facial characteristics, mental retardation, seizures and an inability to suck and/or swallow. Jaundice and gastrointestinal bleeding may also occur."
The new research will open areas for further investigation.
"Before this work in trypanosomes, there was no evidence that we could 'catch' peroxisome proteins moving
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Contact: Kim Carlyle
kcarlyle@uga.edu
706-583-0913
University of Georgia
9-May-2006