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Mitochondrial ribosome recycling factor (MRRF) is an essential component of the mitochondrial translational machinery. It participates in the final step of mitochondrial protein synthesis, mediating the recycling of mitoribosomes—specifically, the dissociation of ribosomes from mRNA at the end of translation. MRRF partners with mitochondrial elongation factor G2 (EF-G2mt) in a process that ensures the proper separation of ribosomal subunits for subsequent rounds of translation, maintaining the integrity of mitochondrial function. MRRF is required for cell viability; depletion leads to aggregation of mitoribosomes, severe mitochondrial structural defects, increased oxidative stress, loss of respiratory complexes, and cell death. The mammalian MRRF is encoded in the nuclear genome and targeted to mitochondria, with unique structural features distinct from both bacterial and chloroplast RRFs. Though not exploited directly by approved drugs, its bacterial homolog is a validated target for antibiotic development.
Inhibition of ribosome recycling and protein synthesis (proposed for antibiotics acting on bacterial RRF)
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