Mitochondrial fatty acid synthesis is best known for producing lipoic acid, however, longer acyl chain products regulate mitochondrial electron transport chain assembly, oxidative TCA cycle metabolism, and skeletal myoblast differentiation.

A high-throughput mitochondrial phenotyping approach quantifies mitochondrial features among purified human immune cell subtypes and provides foundational knowledge to map inter- and intra-individual variation in mitochondrial energetics with high biological specificity.

Animal models reveal that mitochondrial complex I is dispensable for homeostatic functions of the mouse liver.

Transferred mitochondria do not always regulate cell behavior by simply restoring mitochondrial function, but rather, transferred mitochondria are dysfunctional, initiating downstream signaling and proliferation in response to reactive oxygen species.

Cell imaging and electrophysiology in the mouse hippocampus reveal a crucial role for the spatiotemporal regulation of mitochondrial dynamics in PV+ interneurons on cell morphology, network activity, and behavior.

BUD23 links ribosome function with mitochondrial protein expression and efficient oxidative phosphorylation by promoting selective mRNA translation and is therefore critical to mouse development and postnatal cardiac function.

Applied pressure enables efficient isolated mitochondrial transfer and stable mitochondrial DNA (mtDNA) transplantation into a range of mtDNA-depleted cell types to restore respiration.

Missense mutations in the nuclear-encoded adenine nucleotide translocase 1 (Ant1) cause the protein to clog the mitochondrial protein import pathway, to severely inhibit cell growth in yeast, and to cause neurodegeneration and myopathy in mice that phenocopy ANT1-induced human disease.

Identifying 1,907 mitochondrial somatic mutations from 1,675 tumor tissues provides new insights into the causes and effects of the mitochondrial genome mutations found in human cancers.

A quantitative analysis of glucose-dependent transport regulation indicates that mitochondrial accumulation in regions of high nutrient availability can enhance metabolism in neuronal axons under physiologically relevant conditions.