Mitochondrial Function and Pathology

The paper shows that increasing mitochondria-ER contacts in Drosophila improves locomotion, extends lifespan, and reduces Alzheimer's disease symptoms.

This study shows that overexpressing spargel in a Drosophila mitochondrial disease model has minimal effects on phenotype and gene expression.

This study shows that Parl deficiency in mice leads to mitochondrial dysfunction, Complex III defects, and Leigh-like syndrome, highlighting its critical role in neurological health.

The paper introduces MITO-Tag Mice to isolate mitochondria from specific cell types in vivo and identifies mitochondrial metabolite changes during fasting and refeeding in hepatocytes.

The paper uses computational models to show that mitochondrial arrangement affects metabolite distribution and force dynamics in cardiac cells, with implications under hypoxia.

This study uses cryo-electron tomography to show that spatial restrictions in axons and presynaptic varicosities influence mitochondrial morphology and membrane organization.

This study shows psychological stress increases circulating cell-free mitochondrial DNA (ccf-mtDNA) in humans through glucocorticoid signaling, with no change in nuclear DNA levels.

This study shows that axonal mitochondria in C. elegans are necessary for neuropeptide secretion, and that oxidative phosphorylation, not calcium uptake, is required for this process.

This study develops OCR-Stats, a statistical method to improve the accuracy of mitochondrial respiration measurements from Seahorse XF Analyzer data by addressing noise and variation across plates and wells.

The paper examines co-expression of mitochondrial and nuclear OXPHOS genes across human tissues, finding positive co-expression in most tissues but negative correlation in ancient brain regions.

This study shows that high mitochondrial heteroplasmy in mice reduces lifespan and impairs glucose metabolism.

The paper shows that mitochondrial ultrastructure in axons correlates with synaptic performance in mice and humans, indicating activity-dependent plasticity of mitochondria in response to synaptic demand.

This study identifies a homozygous ERAL1 mutation as the cause of Perrault syndrome, showing it disrupts mitochondrial ribosome assembly and function.

The paper shows that knocking down the mitochondrial DNA polymerase Tamas blocks paternal mtDNA loss in Drosophila, suggesting a novel role for DNA polymerase in mtDNA elimination.