Interaction of oncoprotein transcription factor MYC with chromatin-associated protein host cell factor–1 controls expression of genes important for ribosome biogenesis and mitochondrial vigor, loss of which promotes tumor regression.
Comparative -omic analyses of five knockout mouse strains with disrupted mitochondrial DNA expression at different levels provide a high quality resource of altered gene expression patterns that reveal several common secondary patophysiological changes of mitochondrial dysfunction.
Common nuclear genetic variants are associated with fundamental biological processes occurring in human mitochondria and potentially point to novel roles for nuclear genes in transcriptional regulation of the mitochondrial genome.
Building on previous work (Reznik et al., 2016), independent measurements of mitochondrial genome copy number and expression indicate that several solid tumor types suppress respiratory metabolism compared to normal tissue.
Mitochondria can tune the protein synthesis of nuclear-encoded proteins through condition-dependent mRNA localization that is regulated by translation elongation and the geometric constraints of the cell.