Samantha C. Lewis

The paper investigates how mitochondrial architecture changes during mtRNA surveillance failure, revealing stress body formation and spatial reorganization of mitochondrial components.

The paper identifies a mechanism of mitochondrial self-renewal in sensory neurons through asymmetric division, showing mtDNA-rich mitochondria at axon branch points produce mtDNA-depleted daughters.

Cryo-ET of Parkin-expressing U2OS cells shows oligomycin/antimycin depolarization moves some ATP synthase to the inner boundary membrane, abolishes matrix calcium granules, and favors closed prohibitin domes.

The paper shows that saturated lipid stress reduces mtDNA synthesis in human cells by disrupting ER-mitochondria contact sites and fatty acid trafficking, which is reversed by monounsaturated fatty acids.

This study reveals spatial organization of mitochondrial RNA translation and remodeling under stress in human cells.