D. C. Wallace

RESPIRATION DEFECTS LIMIT SERINE SYNTHESIS REQUIRED FOR LUNG CANCER GROWTH AND SURVIVAL

This study shows that mitochondrial DNA mutations in NSCLC cause respiration defects, leading to glucose dependency, reduced serine synthesis, and increased cancer survival.

Post-Transcriptional Methylation of Mitochondrial-tRNA Differentially Contributes to Mitochondrial Pathology

The paper shows that N1-methylation at position 9 of mt-Leu(UAA) stabilizes wild-type mt-tRNA but destabilizes pathogenic variants, suggesting methylation control could be therapeutic.

A mitochondrial surveillance mechanism activated by SRSF2 mutations in hematologic malignancies

This study shows that SRSF2 mutations disrupt mitochondrial mRNA splicing, impair complex I function, and increase mitophagy through a PINK1 splicing mechanism, identifying mitophagy as a therapeutic target in MDS and AML.

Setd2 inactivation sensitizes lung adenocarcinoma to inhibitors of oxidative respiration and mTORC1 signaling

This study shows that SETD2 inactivation in lung adenocarcinoma leads to increased oxidative metabolism and mTORC1 activity, making these tumors sensitive to inhibitors of oxidative respiration and mTORC1.

Nicotinamide Riboside alleviates exercise intolerance in ANT1-deficient mice.

This study shows that nicotinamide riboside improves exercise capacity in ANT1-deficient mice by increasing NAD+ levels and mitochondrial respiration.

SARS-CoV-2 Viroporins Activate The NLRP3-Inflammasome Via The Mitochondrial Permeability Transition Pore

This study shows SARS-CoV-2 viroporins E and Orf3a increase mitochondrial calcium and reactive oxygen species, which activate the NLRP3 inflammasome via the mitochondrial permeability transition pore.

OxPhos Dysfunction Causes Hypermetabolism and Reduces Lifespan in Cells and in Patients with Mitochondrial Diseases

The paper shows that OxPhos dysfunction leads to hypermetabolism and reduced lifespan in cells and mitochondrial disease patients.