The membrane of an animal is comprised of phospholipids which are composed of hydrophobic fatty acid tails and hydrophilic phospholipid head groups. There are many different fatty acid species and phospholipid head groups found in the membrane, and it has been established that proper composition of each is necessary for optimal membrane function. However, it
Because appropriate membrane composition can differ based on the needs of the cell, the membrane has to be able to modulate its makeup when challenged with different stimuli. One of the major challenges to the membrane is that the structure of fatty acid molecules makes them susceptible to attack by reactive oxygen species. The accumulation of damaged lipids in the membrane has a dramatic impact on the membrane’s ability to function, and, therefore, removing damaged fatty acids from the membrane has implications for protecting membrane function. Although an active response to damage has been observed in proteins and nucleic acids, an inducible lipid repair pathway has not been defined. In this project, we will characterize if fatty acid turnover is a lipid repair pathway that aids in the elimination of damaged fatty acids.
In old animals, the relative abundance of fatty acid species in the membrane is dramatically different than in young animals. Specifically, there is an increase in the amount of saturated fatty acids and a depletion of polyunsaturated fatty acids. We have evidence that suggests that decreased membrane turnover in old animals may be insufficient to combat the increased damage seen in aging, resulting in a loss of polyunsaturated fat species and an overall altered membrane composition. We will seek to demonstrate why the membranes have reduced polyunsaturated fatty acids and to address whether this depletion is a cause or contributor to aging and aging-related disease.