, the proteins will be destroyed in the liver or recognized as foreign by the immune system.
When we started, the objective was to look at the genomes of insects, which just started being sequenced, and figure out what glycosylation enzymes they had and what enzymes they were missing so that we could either add on or subtract an enzyme to duplicate the human pathway, she said.
Palter was intrigued by a paper from Jurgen Roth and his colleagues published in 1992, which reported detecting the complex sugars typical of human proteins in insects, but found they were restricted to the cells of the central nervous system.
Unfortunately, researchers did not believe or follow up on Roths initial study, she said. However, I became interested in what the role of complex glycosylation might be in the central nervous system. As a geneticist, I thought we could use the sophisticated genetic approaches available in the fruit fly to understand this.
This led to a second research project, which involves studying mutant flies that lack the ability to add the terminal sugar, sialic acid, to specific proteins of the central nervous system. Mutant flies exhibit abnormal mating behavior, have defects in their ability to fly and climb, and as they age they experience neurodegeneration resulting in seizures and paralysis.
The nerves of the mutant flies are defective in electrical signaling, which impairs their ability to communicate with one another and muscle cells, Palter said. Our mutant flies may provide a model system to study a class of human diseases whose symptoms include memory loss, ataxia, epilepsy and neurodegeneration.
Both of these studies are being done in collaboration with scientists at Johns Hopkins University, the University of Iowa and New York University Medical School, and have been funded through support from the National Institutes of Health. The researchers have published some of tPage: 1 2 3 Related medicine news :1
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