Craig B. Thompson

The paper shows that respiration-deficient cells rely on pyruvate carboxylase to prevent asparagine auxotrophy, with effects dependent on mitochondrial heteroplasmy levels.

The paper introduces mtDIVE, a random mtDNA mutagenesis platform, to study genotype-phenotype associations in metabolic contexts and lineages, revealing lineage-specific effects and mutation-specific impacts.

The paper identifies MTERF1 as a suppressor of mtDNA deletion pathologies by showing its loss enhances mitochondrial function through transcriptional relief.

This study shows that mitochondrial ATP production, induced by D-α-hydroxybutyrate, promotes T cell differentiation and function by regulating chromatin accessibility and gene expression.

This paper develops a method to engineer specific mtDNA deletions in human cells using end-joining machinery and targeted endonucleases, revealing a 75% heteroplasmy threshold for mitochondrial dysfunction.

This study shows lactate activates the mitochondrial electron transport chain without being metabolized, suppressing glycolysis and enhancing oxidative phosphorylation in various cell types.

This study develops a genetic tool to reversibly inhibit miRNA-mediated gene repression in vivo and shows tissue-specific dependencies on miRNA function for homeostasis and regeneration.