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

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

PROVIDER: PRJNA955269 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24163137_1.fastq.gz	Fastqsanger.gz
	SRR24163137_2.fastq.gz	Fastqsanger.gz
	SRR24163138_1.fastq.gz	Fastqsanger.gz
	SRR24163138_2.fastq.gz	Fastqsanger.gz
	SRR24163139_1.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 (tRNA-Seq)

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

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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)

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

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).

2024-01-06 | GSE229672 | GEO

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

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

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

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

2024-01-06 | GSE229673 | GEO

The anti-Shine-Dalgarno sequence drives translational pausing and codon choice in bacteria

Project description:Protein synthesis by ribosomes takes place on a linear substrate but at variable speeds. Transient pausing of ribosomes can impact a variety of co-translational processes, including protein targeting and folding. These pauses are influenced by the sequence of the mRNA. Thus redundancy in the genetic code allows the same protein to be translated at different rates. However, our knowledge of both the position and the mechanism of translational pausing in vivo is highly limited. Here we present a genome-wide analysis of translational pausing in bacteria using ribosome profiling-deep sequencing of ribosome-protected mRNA fragments. This approach enables high-resolution measurement of ribosome density profiles along most transcripts at unperturbed, endogenous expression levels. Unexpectedly, we found that codons decoded by rare tRNAs do not lead to slow translation under nutrient-rich conditions. Instead, Shine-Dalgarno-(SD) like features within coding sequences cause pervasive translational pausing. Using an orthogonal ribosome possessing an altered anti-SD sequence, we demonstrated that pausing is due to hybridization between mRNA and the 16S rRNA of the translating ribosome. In protein coding sequences, internal SD sequences are disfavoured, which leads to biased usage, avoiding codons and codon pairs that resemble canonical SD sites. Our results indicate that internal SD-like sequences are a major determinant of translation rates and a global driving force for the coding of bacterial genomes. Identification of translation pause sites in vivo using ribosome profiling

2012-04-01 | E-GEOD-35641 | biostudies-arrayexpress

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

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

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