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Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming (tRNA-Seq)

ABSTRACT: Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming (tRNA-Seq)

PROVIDER: PRJNA1026841 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26346532.fastq.gz	Fastqsanger.gz
	SRR26346533.fastq.gz	Fastqsanger.gz
	SRR26346534.fastq.gz	Fastqsanger.gz
	SRR26346535.fastq.gz	Fastqsanger.gz
	SRR26346536.fastq.gz	Fastqsanger.gz

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Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming

Project description:Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming

| PRJNA955266 | ENA

Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming (RNA-Seq)

Project description:Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming (RNA-Seq)

| PRJNA955269 | ENA

Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming (Ribosome profiling)

Project description:Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming (Ribosome profiling)

| PRJNA955270 | ENA

Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming (tRNA-Seq)

Project description:To understand the underlying mechanism of YRDC, an enzyme catalysing the formation of N6-threonylcarbamoyladenosine (t6A) on ANN-decoding tRNAs, and the interplay between threonine and YRDC in glioblastoma stem cells (GSCs), we carried out comparative transcriptomic analysis in patient-derived GSC456 with or without YRDC deprivation and with or without threonine restriction (control media, 800 μM threonine; threonine-restricted media, 4 μM). To further investigate the translational regulation of YRDC and threonine in GSCs, we performed ribosome profiling in GSC456 with or without YRDC deprivation and with or without threonine restriction (control media, 800 μM threonine; threonine-restricted media, 4 μM). To investigate the effects of YRDC and threonine purtubation on tRNA expression in GSCs, we performed tRNA sequencing in GSC456 with or without YRDC deprivation and with or without threonine restriction (control media, 800 μM threonine; threonine-restricted media, 4 μM).

2024-01-06 | GSE245043 | GEO

Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming

Project description:Cancers commonly reprogram translation and metabolism, but little is known about how these two features coordinate in cancer stem cells. Here, we show that glioblastoma stem cells (GSCs) display elevated protein translation. To dissect underlying mechanisms, we performed a CRISPR screen and identified YRDC as the top essential tRNA modification enzymes in GSCs. YRDC catalyses the formation of N6-threonylcarbamoyladenosine (t6A) on ANN-decoding tRNAs (A denotes adenosine and N denotes any nucleotide). Targeting YRDC reduced t6A formation, suppressed global translation, and inhibited tumour growth both in vitro and in vivo. Threonine is an essential substrate of YRDC. Threonine accumulated in GSCs, which facilitated t6A formation through YRDC and shifted the proteome to support mitosis-related genes with ANN codon-bias. Dietary threonine restriction (TR) reduced tumour t6A formation, slowed xenograft growth, and augmented anti-tumour efficacy of chemotherapy and anti-mitotic therapy, providing a molecular basis for a dietary intervention in cancer treatment.

2024-02-22 | PXD049966 | Pride

Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming (Ribosome profiling)

2024-01-06 | GSE229672 | GEO

Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming (RNA-Seq)

2024-01-06 | GSE229671 | GEO

Threonine fuels glioblastoma through YRDC-mediated codon-biased translational reprogramming

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-06 | GSE229673 | GEO

A snoRNA–tRNA modification network governs codon-biased cellular states

Project description:A snoRNA–tRNA modification network governs codon-biased cellular states

| PRJNA982754 | ENA

A snoRNA–tRNA modification network governs codon-biased cellular states

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 | GSE234689 | GEO

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