The heme and HRI-mediated eIF2aP–ATF4 integrated stress response in erythropoiesis has a major global impact, especially under the stress condition of iron deficiency.

BUD23 links ribosome function with mitochondrial protein expression and efficient oxidative phosphorylation by promoting selective mRNA translation and is therefore critical to mouse development and postnatal cardiac function.

Structural analysis of translating human mitoribosome illustrates elemental steps of translation in mitochondria.

Missense mutations in the nuclear-encoded adenine nucleotide translocase 1 (Ant1) cause the protein to clog the mitochondrial protein import pathway, to severely inhibit cell growth in yeast, and to cause neurodegeneration and myopathy in mice that phenocopy ANT1-induced human disease.

Asc1/RACK1 promotes the translation of mRNAs associated with the translational closed loop complex, which have short open reading frames and encode proteins required for core metabolic processes.

Tom70 connects the mitochondrial import to the nuclear transcriptional activity of mitochondrial proteins and controls mitochondrial biogenesis defects during aging.

The ciliate mitoribosome structure provides new insights into the diversity of translation and its evolution.

Plants and humans use a shared mechanism, the eukaryotic metabolic sensor TARGET OF RAPAMYCIN protein kinase and its substrate, an RNA-binding protein called LARP1, to coordinate post-transcriptional gene expression.

The Bi-Genomic Mitochondrial-Split-GFP, where both fragments of the Split-GFP are expressed by separated translation machineries, shuts off cytosolic fluorescence of dual-localized proteins, allowing visualization of their mitochondrial echoforms.

Induction of the fission of mitochondria-populating sensory axons is shown to be a novel biological action of neurotrophins.