Ruobing Cui

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 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.