M6A is decoded by modified tRNAs to coordinate mRNA decay [Quant-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1235615 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32679355.fastq.gz | Fastqsanger.gz | |||
| SRR32679356.fastq.gz | Fastqsanger.gz | |||
| SRR32679357.fastq.gz | Fastqsanger.gz | |||
| SRR32679358.fastq.gz | Fastqsanger.gz | |||
| SRR32679359.fastq.gz | Fastqsanger.gz |
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Project description:Chemically modified mRNA nucleotides are emerging as key regulators of gene expression. Their effects are typically thought to be mediated through reader proteins that selectively bind to RNA molecules containing these modifications. Here, we present a new mechanism by which N6 methyladenosine (m6A) couples the translation of messenger RNA (mRNA) to its decay. m6A-modified codons are decoded inefficiently by the ribosome, rendering them “non-optimal”. At these codons, m6A slows down elongating ribosomes and thereby triggers translation-dependent decay of the mRNA. Inefficient decoding of m6A-modified codons is counteracted by the transfer RNA (tRNA) anticodon modification 5-methoxycarbonylmethyl-2-thiouridine (mcm5s2U). mcm5s2U increases the decoding efficiency of a subset of m6A codons and thereby alleviates m6A-mediated mRNA decay. This unanticipated link between the mRNA and tRNA epitranscriptomes controls the decay of mRNAs of important oncogenic signaling pathways. The biogenesis of m6A and mcm5s2U is coordinated in normal tissues but dysregulated in cancer, where a shift towards more mcm5s2U stabilizes these RNAs and is associated with higher tumor aggressiveness and poor prognosis. Thus, the balance between m6A and mcm5s2U acts as a pan-epitranscriptomic mechanism that regulates gene expression and curtails tumorigenesis.
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Project description:In eukaryotes, the genetic code is transcribed into messenger RNA (mRNA) in the nucleus and decoded by transfer RNA (tRNA) in the cytosol. Nuclear mRNA processing events that do not affect the nucleotide sequence of an mRNA are thought to be invisible to tRNAs during protein translation in the cytosol. Here, we report a mechanism by which the modified mRNA nucleotide N6‑methyladenosine (m6A) connects nuclear mRNA processing to tRNA decoding. m6A is deposited in the protein coding sequence (CDS) of mRNAs with long exons, where it slows the decoding of a subset of m6A-modified codons in vivo. Translation of codons with m6A at the wobble position is facilitated by 5-methoxycarbonylmethyl-2-thiouridine (mcm5s2U), a modified nucleotide of the tRNA anticodon loop that juxtaposes the wobble-m6A. This unanticipated link between the mRNA and tRNA epitranscriptomes controls mRNA half-life in a translation-dependent manner and connects the exon-intron architecture of mRNAs to their turnover. The pathways for m6A and mcm5s2U biogenesis are tightly co-regulated in human tissues but deregulated in cancer cells. In breast cancer, a shift towards more mcm5s2U is associated with tumor aggressiveness and poor prognosis. Thus, the m6A/mcm5s2U-balance has evolved as a pan-epitranscriptomic mechanism that coordinates gene expression changes and curtails tumorigenesis.
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Project description:Chemically modified mRNA nucleotides are emerging as key regulators of gene expression. Their effects are typically thought to be mediated through reader proteins that selectively bind to RNA molecules containing these modifications. Here, we present a new mechanism by which N6 methyladenosine (m6A) couples the translation of messenger RNA (mRNA) to its decay. m6A-modified codons are decoded inefficiently by the ribosome, rendering them “non-optimal”. At these codons, m6A slows down elongating ribosomes and thereby triggers translation-dependent decay of the mRNA. Inefficient decoding of m6A-modified codons is counteracted by the transfer RNA (tRNA) anticodon modification 5-methoxycarbonylmethyl-2-thiouridine (mcm5s2U). mcm5s2U increases the decoding efficiency of a subset of m6A codons and thereby alleviates m6A-mediated mRNA decay. This unanticipated link between the mRNA and tRNA epitranscriptomes controls the decay of mRNAs of important oncogenic signaling pathways. The biogenesis of m6A and mcm5s2U is coordinated in normal tissues but dysregulated in cancer, where a shift towards more mcm5s2U stabilizes these RNAs and is associated with higher tumor aggressiveness and poor prognosis. Thus, the balance between m6A and mcm5s2U acts as a pan-epitranscriptomic mechanism that regulates gene expression and curtails tumorigenesis.
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Project description:Chemically modified mRNA nucleotides are emerging as key regulators of gene expression. Their effects are typically thought to be mediated through reader proteins that selectively bind to RNA molecules containing these modifications. Here, we present a new mechanism by which N6 methyladenosine (m6A) couples the translation of messenger RNA (mRNA) to its decay. m6A-modified codons are decoded inefficiently by the ribosome, rendering them “non-optimal”. At these codons, m6A slows down elongating ribosomes and thereby triggers translation-dependent decay of the mRNA. Inefficient decoding of m6A-modified codons is counteracted by the transfer RNA (tRNA) anticodon modification 5-methoxycarbonylmethyl-2-thiouridine (mcm5s2U). mcm5s2U increases the decoding efficiency of a subset of m6A codons and thereby alleviates m6A-mediated mRNA decay. This unanticipated link between the mRNA and tRNA epitranscriptomes controls the decay of mRNAs of important oncogenic signaling pathways. The biogenesis of m6A and mcm5s2U is coordinated in normal tissues but dysregulated in cancer, where a shift towards more mcm5s2U stabilizes these RNAs and is associated with higher tumor aggressiveness and poor prognosis. Thus, the balance between m6A and mcm5s2U acts as a pan-epitranscriptomic mechanism that regulates gene expression and curtails tumorigenesis.
2025-05-09 | GSE247664 | GEO
Project description:Chemically modified mRNA nucleotides are emerging as key regulators of gene expression. Their effects are typically thought to be mediated through reader proteins that selectively bind to RNA molecules containing these modifications. Here, we present a new mechanism by which N6 methyladenosine (m6A) couples the translation of messenger RNA (mRNA) to its decay. m6A-modified codons are decoded inefficiently by the ribosome, rendering them “non-optimal”. At these codons, m6A slows down elongating ribosomes and thereby triggers translation-dependent decay of the mRNA. Inefficient decoding of m6A-modified codons is counteracted by the transfer RNA (tRNA) anticodon modification 5-methoxycarbonylmethyl-2-thiouridine (mcm5s2U). mcm5s2U increases the decoding efficiency of a subset of m6A codons and thereby alleviates m6A-mediated mRNA decay. This unanticipated link between the mRNA and tRNA epitranscriptomes controls the decay of mRNAs of important oncogenic signaling pathways. The biogenesis of m6A and mcm5s2U is coordinated in normal tissues but dysregulated in cancer, where a shift towards more mcm5s2U stabilizes these RNAs and is associated with higher tumor aggressiveness and poor prognosis. Thus, the balance between m6A and mcm5s2U acts as a pan-epitranscriptomic mechanism that regulates gene expression and curtails tumorigenesis.
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