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Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [RiboSeq]

ABSTRACT: Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [RiboSeq]

PROVIDER: PRJNA757962 | ENA |

REPOSITORIES: ENA

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Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [RiboSeq]

Project description:Oligodendrocytes are specialized cells that confer neuronal myelination. Leukodystrophies associated with oligodendrocyte and hypomyelination are known to result when a number of tRNA metabolism genes are mutated. Thus, for unknown reasons, oligodendrocytes may be hypersensitive to perturbations in tRNA biology. In this study, we survey the tRNA transcriptome in the murine oligodendrocytes cell lineage in an effort to understanding the molecular underpinning for human disease. We find that specific tRNAs are hypomodified in oligodendrocytes within or near the anticodon. This hypomodified state may be the result of differential expression of key modification enzymes during oligodendrocyte differentiation. Moreover, we observe a concomitant relationship between tRNA hypomodification and tRNA decoding potential; observing oligodendrocyte specific alterations in codon optimality-mediated mRNA decay and ribosome transit. Our results reveal that oligodendrocytes naturally maintain a delicate, hypersensitized tRNA/mRNA axis. We suggest this axis underlies disease etiology when further insult to tRNA metabolism is introduced.

2022-08-08 | GSE182810 | GEO

Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [DecaySeq]

2022-08-08 | GSE182809 | GEO

Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [QuantMseq]

2022-08-08 | GSE182808 | GEO

Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [QuantM-seq II]

2022-08-08 | GSE198271 | GEO

Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay

Project description:Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay

| PRJNA757956 | ENA

Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [DecaySeq]

Project description:Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [DecaySeq]

| PRJNA757961 | ENA

Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [QuantMseq]

Project description:Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [QuantMseq]

| PRJNA757960 | ENA

Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [QuantM-seq II]

Project description:Oligodendrocyte differentiation alters tRNA modifications and codon-dependent mRNA decay [QuantM-seq II]

| PRJNA814310 | ENA

A snoRNA–tRNA modification network governs codon-biased cellular states [RNAseq & Riboseq]

Project description:A snoRNA–tRNA modification network governs codon-biased cellular states [RNAseq & Riboseq]

| PRJNA982760 | ENA

A snoRNA–tRNA modification network governs codon-biased cellular states [RNAseq & Riboseq]

Project description:The dynamic balance between tRNA supply and codon usage demand is a fundamental principle in the cellular translation economy. However, the regulation and functional consequences of this balance remain unclear. Here, we use PARIS2 interactome capture, structure modeling, conservation analysis, RNA–protein interaction analysis, and modification mapping to reveal the targets of hundreds of snoRNAs, many of which were previously considered orphans. We identify a snoRNA–tRNA interaction network that is required for global tRNA modifications, including 2′-O-methylation and others. Loss of Fibrillarin, the snoRNA-guided 2′-O-methyltransferase, induces global upregulation of tRNA fragments, a large group of regulatory RNAs. In particular, the snoRNAs D97/D133 guide the 2′-O-methylation of multiple tRNAs, especially for the amino acid methionine (Met), a protein-intrinsic antioxidant. Loss of D97/D133 snoRNAs in human HEK293 cells reduced target tRNA levels and induced codon adaptation of the transcriptome and translatome. Both D97/D133 single and double knockouts in HEK293 cells suppress Met-enriched proliferation-related gene expression programs, including, translation, splicing, and mitochondrial energy metabolism, and promote Met-depleted programs related to development, differentiation, and morphogenesis. In a mouse embryonic stem cell model of development, knockdown and knockout of D97/D133 promote differentiation to mesoderm and endoderm fates, such as cardiomyocytes, without compromising pluripotency, consistent with the enhanced development-related gene expression programs in human cells. This work solves a decade-old mystery about orphan snoRNAs and reveals a function of snoRNAs in controlling the codon-biased dichotomous cellular states of proliferation and development.

2023-09-21 | GSE234687 | GEO

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