Two teams of scientists, publishing online in Nature, have revealed that a mutant protein implicated in inherited Parkinson's disease disables the cell's mitochondria, a finding that underscores the importance of the energy-generating organelles in the neurodegenerative disorder.
Previously, scientists had shown that a familial form of Parkinson's that strikes early in life is caused by mutations in the PTEN-induced putative kinase 1 (PINK1) gene. Now, teams led by Jongkyeong Chung and Ming Guo have explored what this gene does by studying the equivalent gene in the fruitfly, Drosophila.
The teams show that flies without a functional PINK1 gene suffer defects in mitochondria that appear to trigger muscle problems and, according to Chung's team, degeneration of dopaminergic neurons. The researchers also show that the PINK1 protein acts upstream of Parkin, another molecule underlying sporadic forms of Parkinson's, and that the two proteins most likely act in a common pathway involved in maintaining mitochondrial function. The mutant flies could now be used to find other genes in this pathway via genetic screens.
Ming Guo (UCLA, Los Angeles, CA, USA)
Jongkyeong Chung (Korea Advanced Institute of Science and Technology, Taejon, Republic of Korea)
Abstracts available online:
(C) Nature press release.
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