Updated project metadata. The prokaryotic translation elongation factor P (EF-P), and the eukaryotic/archeal counterparts eIF5A/aIF5A, are proteins that serve a crucial role in mitigating ribosomal stalling during the translation of specific sequences, notably those containing consecutive proline residues. Although mitochondrial DNA-encoded proteins synthesized by mitochondrial ribosomes also contain polyproline stretches, an EF-P/eIF5A mitochondrial counterpart remains unidentified. Here, we show that the missing factor is the translational activator of COX1 (TACO1), a protein causative of a juvenile form of neurodegenerative Leigh's syndrome associated with cytochrome c oxidase deficiency. By using a combination of metabolic labeling, puromycin release, and ribosome profiling experiments, we show that TACO1 is required for the rapid synthesis of the poly-proline rich COX1 and COX3 proteins, while its requirement is negligible for other proteins. In agreement with a role in translation rate regulation, we show that TACO1 cooperates with the N-terminal extension of the large ribosomal subunit bL27m to provide stability to the peptidyl-transferase center during elongation, and that excess TACO1 enhances overall translation rate. We conclude that TACO1 is a Translation Accelerator and propose it as a promising target to regulate mitochondrial protein synthesis in disease scenarios.