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We are interested in understanding the molecular and cell biology that underlies aging. To do this, we use fruit fly as a model organism. A current idea for what drives aging is that organisms are unable to maintain function due to a buildup of damaged biomolecules (like proteins). Mitochondria are particularly important organelles for aging--we think mitochondria are the source of free radicals that cause damage that results in aging, and mitochondria are also the organelle that is expected to be most affected by free radical damage.
Our lab is interested in investigating the role that mitochondrial protein damage plays in aging. Recently, we found that some flies that are healthier and live longer have more robust mitochondrial protein degradation. We don't yet know if this is something that is common to all healthier/longer lived flies. During the summer, we are interested in overexpressing genes that are expected to increase protein degradation in mitochondria. Assessing their effects on mitochondrial functions (i.e. mitochondrial protein degradation, Krebs cycle, electron transport, mitochondrial volume) and fly health (resistance to various stresses, motility, longevity) will provide a direct test of whether boosting mitochondrial protein degradation can be sufficient to increase health and longevity. These results will help us understand whether mitochondrial function is a limiting factor for aging and longevity.