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0 reviewsSUMMARYChemically modified nucleotides in mRNA are critical regulators of gene expression, primarily throughinteractions with reader proteins that bind to these modifications. Here, we present a mechanism bywhich the epitranscriptomic mark N6-methyladenosine (m6A) is read by tRNAs during translation. Codonsthat are modified with m6A are decoded inefficiently by the ribosome, rendering them ‘‘non-optimal’’and inducing ribosome collisions on cellular transcripts. This couples mRNA translation to decay.5-Methoxycarbonylmethyl-2-thiouridine (mcm5s2U) in the tRNA anticodon loop counteracts this effect.This unanticipated link between the mRNA and tRNA epitranscriptomes enables the coordinated decay ofmRNA regulons, including those encoding oncogenic signaling pathways. In cancer, dysregulation of them6A and mcm5s2U biogenesis pathways—marked by a shift toward more mcm5s2U—is associated withmore aggressive tumors and poor prognosis. Overall, this pan-epitranscriptomic interaction represents anovel mechanism of post-transcriptional gene regulation with implications for human health.
