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In a recent paper published by Akabane et al. [1], a homologous mitochondrial translation system was supplemented with ICT1, the mitochondrial translation release factor family member. Under these conditions, ICT1 was shown to exhibit general release activity at all codons tested, including AGA/AGG, which are normally redundant in human mitochondria. The authors suggest that this ICT1 activity may occur in vivo, challenging Temperley et al., 2010 [2]. We wish to point out, however, that the data presented in this paper are in vitro and do not account for the live cell data consistent with a -1 frameshift at AGA/AGG placing a standard UAG stop codon in the human mitoribosomal A-site.

Response to “Ribosome Rescue and Translation Termination at Non-standard Stop Codons by ICT1 in Mammalian Mitochondria”