Abstract 2676 Cascading effects of aspartate limitation during mitochondrial dysfunction

Mitochondria serve as critical metabolic hubs, supporting cell function through both catabolic and anabolic processes. We and others have demonstrated that mitochondrial dysfunction can impair cell proliferation by disrupting aspartate synthesis, however the mechanisms by which aspartate depletion impacts cell proliferation remains poorly understood. Using a newly described aspartate biosensor, live cell imaging, and metabolomics, we reveal cascading metabolic consequences for how changes to aspartate upon mitochondrial impairments can affect downstream metabolism and cell function - and how additional metabolic variables can govern these outcomes.