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Mouse genetic model for spongiform brain diseases

d one escape from the laboratory -- would not get spongiform encephalopathy."

The researchers were looking for effects that might be linked to mutations in pigmentation genes. They knew that a loss of function in the so-called Mahogunin gene causes a partial reduction in the amount of yellow pigment, so that the mice were left with only small patches of yellow hair on mostly black bodies. But they were surprised to learn that a complete loss of function in that gene produced all-black mice with brain neurodegeneration. Linkages between unusual pigmentation and neural defects are not unheard of in the animal world, Gunn adds, citing predominantly white dogs, such as Dalmatians, that sometimes are deaf.

As an animal model, the mahoganoid mutant mice probably will not be useful to study spongiform encephalopathies like mad cow disease, Gunn believes, because rogue prions are not the cause of the mouse condition. But as an example of defective ubiquitination -- a protein-related process involved in many neurodegenerative disorders, including Parkinson's and Alzheimer's diseases -- the mahogany-colored mice with spongy brains could have real value, according to the Cornell scientist.

And the mutant mouse probably isn't patentable because it has a naturally occurring defect that the researchers did not create and because the mice already are commercially available. However, Gunn suggests, further work with the gene responsible for the neurodegenerative condition might result in patent applications.

Gunn credits Cornell undergraduate student Aaron F. Jolly for his research assistance in the study. Jolly is one of eight co-authors of the Science report. The study was supported, in part, by grants from the National Institutes of Health and the American Heart Association.


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Contact: Roger Segelken
hrs2@cornell.edu
607-255-9736
Cornell University News Service
30-Jan-2003


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