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RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells.

ABSTRACT: RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells.

PROVIDER: PRJNA761360 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15738875_1.fastq.gz	Fastqsanger.gz
	SRR15738875_2.fastq.gz	Fastqsanger.gz
	SRR15738876_1.fastq.gz	Fastqsanger.gz
	SRR15738876_2.fastq.gz	Fastqsanger.gz
	SRR15738877_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells

Project description:RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells

| PRJNA903102 | ENA

RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells.

Project description: Not available

| S-EPMC9870888 | biostudies-literature

RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells

Project description:Embryonic stem cell (ESC) fate decisions are regulated by a complex molecular circuitry that requires tightly coordinated gene expression regulations at multiple levels from chromatin organization to mRNA processing. Recently, ribosome biogenesis and translation have emerged as key pathways that efficiently control stem cell homeostasis. However, the molecular mechanisms underlying the regulation of these pathways remain largely unknown to date. Here, we analyzed the expression of over 300 genes involved in ribosome biogenesis between self-renewing and differentiated mouse ESCs. We identified RSL24D1 as highly expressed in multiple mouse pluripotent stem cell models and showed that its expression profile is conserved in human ESCs. RSL24D1 is associated with nuclear pre-ribosomes and is required for the maturation and the biogenesis of 60S subunits in mouse ESCs. Interestingly, RSL24D1 depletion resulted in a significant modification of ESC’s proteome by impairing global translation, particularly of key pluripotency factors, including POU5F1 and NANOG, as well as components of the polycomb repressive complex 2 (PRC2). Consistently, while having a moderate impact on lineage commitment and cell differentiation, RSL24D1 depletion significantly altered mouse ESC self-renewal and proliferation, a phenotype largely alleviated by RSL24D1 knockdown rescue. Taken together, these results demonstrate that RSL24D1-dependant ribosome biogenesis is both required to sustain the expression of pluripotent transcriptional programs and to silence PRC2-dependant developmental programs, which concertedly dictate ESC homeostasis.

2023-01-07 | GSE218290 | GEO

RSL24D1 sustains steady-state ribosome biogenesis and pluripotency translational programs in embryonic stem cells.

Project description:Embryonic stem cell (ESC) fate decisions are regulated by a complex molecular circuitry that requires tight and coordinated gene expression regulations at multiple levels from chromatin organization to mRNA processing. Recently, ribosome biogenesis and translation have emerged as key pathways that efficiently control stem cell homeostasis. However, the molecular mechanisms underlying the regulation of these pathways remain largely unknown to date. Here, we analyzed the expression, in mouse ESCs, of over 300 genes involved in ribosome biogenesis and we identified RSL24D1 as the most differentially expressed between self-renewing and differentiated ESCs. RSL24D1 is highly expressed in multiple mouse pluripotent stem cell models and its expression profile is conserved in human ESCs. RSL24D1 is associated with nuclear pre-ribosomes and is required for the maturation and the synthesis of 60S subunits in mouse ESCs. Interestingly, RSL24D1 depletion significantly impairs global translation, particularly of key pluripotency factors, including POU5F1 and NANOG, as well as components of the polycomb repressive complex 2 (PRC2). Consistently, RSL24D1 is required for mouse ESC self-renewal and proliferation. Taken together, we show that RSL24D1-dependant ribosome biogenesis is required to both sustain the expression of pluripotent transcriptional programs and silence developmental programs, which concertedly dictate ESC homeostasis.

2024-09-06 | GSE183586 | GEO

Wdr4-mediated m7G modification on let-7 miRNA to Maintain Steady-State Ribosome Biogenesis for Intestinal Homeostasis

Project description:Ribosome biogenesis is recently known to control stem cell fate, while its role and regulation in intestinal stem cells (ISCs) remain unexplored. Here, we report that WD repeat protein 4 (Wdr4) complexes with Mettl1, an RNA methyltransferase, mediates m7G modification to preserve steady-state ribosome biogenesis in ISCs of the Drosophila midgut, functional equivalent to mammalian small intestines. Diminishing Wdr4 or Mettl1 elevates ribosome biogenesis, driving ISC overprolifaeration and misdifferentiation, leading to short lifespan. Mechanistically, Wdr4 or Mettl1 depletion in ISCs reduces m 7 G levels and let-7 expression, resulting in increased TOR signaling and ROS levels, which activate the JNK-dMyc signaling cascade. Concurrently, TOR signaling and dMyc enhance ribosome biogenesis. Furthermore, overexpression of human WDR4 and METTL1 in fly ISCs respectively restores the phenotypes caused by Wdr4 and Mettl1 loss, indicating a conserved role of m7G modification to maintain ISC homeostasis across species. Together, our findings unravel miRNA modulation in growth signaling and ribosome biogenesis for ISC homeostasis, offering new avenues for therapeutic interventions.

2025-09-12 | GSE298087 | GEO

Ribosome biogenesis mediates the translational increase of codon non-optimal transcripts during IFN stimulation

Project description:Ribosome biogenesis mediates the translational increase of codon non-optimal transcripts during IFN stimulation

| PRJNA1185811 | ENA

Post-transcriptional regulation of Ribosome Biogenesis

Project description:Post-transcriptional regulation of Ribosome Biogenesis

| PRJNA970342 | ENA

Ribosome profiling of early zebrafish embryos -- miRNA-mediated regulation during embryogenesis causes translational repression before mRNA decay

Project description:MicroRNAs regulate gene expression through deadenylation, repression and mRNA decay. However, the contribution of each mechanism in non-steady-state situations remains unclear. We monitored the impact of miR-430 on ribosome occupancy of endogenous mRNAs in wild type and dicer mutants lacking mature miR-430. Our results indicate that miR-430 reduces the number of ribosomes on target mRNAs before causing mRNA decay. Translational repression occurs before complete deadenylation, and disrupting deadenylation using an internal poly(A) tail did not block target repression. Finally, we observe that ribosome density along the length of the target mRNA remains constant, suggesting that translational repression occurs by reducing the initiation rate rather than reducing elongation or causing ribosomal drop-off. In summary, our results show that miR-430 regulates translation initiation before inducing mRNA decay. Time course parallel ribosome profiling and input mRNA quantification in wildtype and MZdicer mutant embryos

2012-03-15 | E-GEOD-34743 | biostudies-arrayexpress

The E3 SUMO ligase Mms21 controls ribosome biogenesis

Project description:The budding yeast E3 SUMO ligase Mms21, a component of the Smc5-6 complex, regulates sister chromatid cohesion, DNA replication, and DNA repair. We identify a role for Mms21 in ribosome biogenesis. The mms21RINGD mutant exhibits reduced rRNA production, nuclear accumulation of 60S and 40S ribosomal proteins, and elevated Gcn4 translation. Genes involved in ribosome biogenesis and translation are down-regulated in the mms21RINGD mutant. Examining gene expression profile of mms21RINGD mutant compared to wild-type by RNA Seq using Ilumina sequencing

2015-06-13 | E-GEOD-69826 | biostudies-arrayexpress

Ribosome biogenesis mediates the translational increase of non-optimal codon transcripts during IFN stimulation

Project description:The interferon response is a signaling pathway unique to vertebrates that links the innate and adaptive immune responses. Interferons signal through a cascade of factors including the JAK-STAT pathway to induce the transcription of hundreds of interferon stimulated genes (ISGs). Although the main interferon signal transduction pathways and ISGs have been elucidated, translational regulation of ISG transcripts has not been fully investigated. Prior work demonstrated that ribosomal protein RPL28 negatively regulates a subset of ISGs; however, we find that this effect may be due to a reduction in overall ribosome availability. Multi-omics analysis of RNA-seq and LC-MS/MS data reveal proteins that are translationally up-regulated in IFN-β-stimulated cells depleted of ribosome biogeneis factor BOP1, including an enrichment of ISGs. Analysis of codon usage demonstrates a significant reduction in codon optimality for proteins that are translationally up-regulated during BOP1 knockdown and IFN-β stimulation. Using reporter constructs, we demonstrate that codon non-optimal reporters are translated more that codon-optimized reporters in BOP1-depleted IFN-β cells. We propose that ribosome biogenesis regulates translational fine-tuning of integral protein production to ensure optimal interferon responses.

2026-04-30 | PXD060209 | Pride

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