Orthologues, and , Can Suppress -Dependent Age-Related Phenotypes in Drosophila.

The relationship of Amyotrophic Lateral Sclerosis, Parkinson's disease, and other age-related neurodegenerative diseases with mitochondrial dysfunction has led to our study of the mitochondrial fission gene in and aspects of aging. Previously, the Drp1 protein has been demonstrated to interact with the Drosophila Bcl-2 mitochondrial proteins, and mutations can lead to mitochondrial dysfunction and neuronal loss. In this study, the () transgene was exploited to direct the expression of and transgenes in select neurons. Here, the knockdown of seems to compromise locomotor function throughout life but does not alter longevity. The co-expression of suppresses the poor climbing induced by the knockdown of the function. The consequences of overexpression, which specifically reduced median lifespan and diminished climbing abilities over time, can be suppressed through the directed co-overexpression of pro-survival gene or by the co-knockdown of the pro-cell death homologue . Alteration of the expression of acts to phenocopy neurodegenerative disease phenotypes in Drosophila, while overexpression of can counteract or rescue these phenotypes to improve overall health. The diminished healthy aging due to either the overexpression of or the RNA interference of has produced novel Drosophila models for investigating mechanisms underlying neurodegenerative disease.