RNA helicase DDX10 is Required for Pluripotency of Stem Cells by Regulating 18S rRNA Processing
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ABSTRACT:
PROVIDER: PRJNA970810 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24488163.fastq.gz | Fastqsanger.gz | |||
| SRR24488164.fastq.gz | Fastqsanger.gz | |||
| SRR24489382_1.fastq.gz | Fastqsanger.gz | |||
| SRR24489382_2.fastq.gz | Fastqsanger.gz | |||
| SRR24489383_1.fastq.gz | Fastqsanger.gz |
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Project description:Ribosomes, as a protein synthesis machine, are required for stem cells to maintain self-renewal. Here, we find that DEAD-box RNA helicase DDX10 is necessary for cellular pluripotency acquisition in somatic cell reprogramming, and in mouse embryonic stem cells (mESCs), DDX10 degradation disrupts cellular homeostasis, leads to cell cycle arrest in G1 phase and markedly inhibits cell proliferation. DDX10 is localized in dense fiber component (DFC) and granular component (GC), mainly binds to 45S ribosomal RNA (rRNA) and participates in regulating ribosome biogenesis. Specifically, DDX10 degradation prevents the release of U3 snoRNA from pre-rRNA, and disrupts pre-rRNA processing and maturation of 18S rRNA, leading to impaired ribosomal small subunit production. Together, this study reveals that DDX10 functions as an important regulator of ribosome biogenesis, and is essential for the survival, induction and maintenance of pluripotent stem cells.
2024-10-15 | GSE232092 | GEO
Project description:Ribosomes, as a protein synthesis machine, are required for stem cells to maintain self-renewal. Here, we find that DEAD-box RNA helicase DDX10 is necessary for cellular pluripotency acquisition in somatic cell reprogramming, and in mouse embryonic stem cells (mESCs), DDX10 degradation disrupts cellular homeostasis, leads to cell cycle arrest in G1 phase and markedly inhibits cell proliferation. DDX10 is localized in dense fiber component (DFC) and granular component (GC), mainly binds to 45S ribosomal RNA (rRNA) and participates in regulating ribosome biogenesis. Specifically, DDX10 degradation prevents the release of U3 snoRNA from pre-rRNA, and disrupts pre-rRNA processing and maturation of 18S rRNA, leading to impaired ribosomal small subunit production. Together, this study reveals that DDX10 functions as an important regulator of ribosome biogenesis, and is essential for the survival, induction and maintenance of pluripotent stem cells.
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Project description:RNA helicase DDX10 is Required for Pluripotency of Stem Cells by Regulating 18S rRNA Processing (RNA-Seq)
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Project description:RNA helicase DDX10 is Required for Pluripotency of Stem Cells by Regulating 18S rRNA Processing (CLIP-Seq)
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Project description:This SuperSeries is composed of the SubSeries listed below.
2024-10-14 | GSE232096 | GEO
Project description:Ribosome biogenesis is essential for protein synthesis in gene expression. Yeast eIF5B has been shown biochemically to facilitate 18S rRNA 3’ end maturation during late-40S ribosomal subunit assembly and gate the transition from translation initiation to elongation. But the effects of eIF5B have not been studied at the genome-wide level in any organism, and 18S rRNA 3’ end maturation is poorly understood in plants. Arabidopsis HOT3/eIF5B1 was found to promote development and heat-stress acclimation by translational regulation, but its molecular function remained unknown. Here, we show that HOT3 is a late-stage ribosome biogenesis factor that facilitates 18S rRNA 3’ end processing and is a translation initiation factor that globally impacts the transition from initiation to elongation. By developing and implementing 18S-ENDseq, we revealed previously unknown events in 18S rRNA 3’ end maturation or metabolism. We quantitatively defined new processing hotspots and identified adenylation as the prevalent non-templated RNA modification at the 3’ ends of pre-18S rRNAs. Aberrant 18S rRNA maturation in hot3 further activated RNAi to generate RDR1- and DCL2/4-dependent risiRNAs mainly from a 3’ portion of 18S rRNA. We further showed that risiRNAs in hot3 were predominantly localized in ribosome-free fractions not responsible for the 18S rRNA maturation or translation initiation defects in hot3. Our study uncovered the molecular function of HOT3/eIF5B1 in 18S rRNA maturation at the late-40S assembly stage and revealed the regulatory crosstalk among ribosome biogenesis, mRNA translation initiation, and siRNA biogenesis in plants.
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Project description:Ribosome biogenesis is essential for protein synthesis in gene expression. Yeast eIF5B has been shown biochemically to facilitate 18S rRNA 3’ end maturation during late-40S ribosomal subunit assembly and gate the transition from translation initiation to elongation. But the effects of eIF5B have not been studied at the genome-wide level in any organism, and 18S rRNA 3’ end maturation is poorly understood in plants. Arabidopsis HOT3/eIF5B1 was found to promote development and heat-stress acclimation by translational regulation, but its molecular function remained unknown. Here, we show that HOT3 is a late-stage ribosome biogenesis factor that facilitates 18S rRNA 3’ end processing and is a translation initiation factor that globally impacts the transition from initiation to elongation. By developing and implementing 18S-ENDseq, we revealed previously unknown events in 18S rRNA 3’ end maturation or metabolism. We quantitatively defined new processing hotspots and identified adenylation as the prevalent non-templated RNA modification at the 3’ ends of pre-18S rRNAs. Aberrant 18S rRNA maturation in hot3 further activated RNAi to generate RDR1- and DCL2/4-dependent risiRNAs mainly from a 3’ portion of 18S rRNA. We further showed that risiRNAs in hot3 were predominantly localized in ribosome-free fractions not responsible for the 18S rRNA maturation or translation initiation defects in hot3. Our study uncovered the molecular function of HOT3/eIF5B1 in 18S rRNA maturation at the late-40S assembly stage and revealed the regulatory crosstalk among ribosome biogenesis, mRNA translation initiation, and siRNA biogenesis in plants.
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Project description:Ribosome biogenesis is essential for protein synthesis in gene expression. Yeast eIF5B has been shown biochemically to facilitate 18S rRNA 3’ end maturation during late-40S ribosomal subunit assembly and gate the transition from translation initiation to elongation. But the effects of eIF5B have not been studied at the genome-wide level in any organism, and 18S rRNA 3’ end maturation is poorly understood in plants. Arabidopsis HOT3/eIF5B1 was found to promote development and heat-stress acclimation by translational regulation, but its molecular function remained unknown. Here, we show that HOT3 is a late-stage ribosome biogenesis factor that facilitates 18S rRNA 3’ end processing and is a translation initiation factor that globally impacts the transition from initiation to elongation. By developing and implementing 18S-ENDseq, we revealed previously unknown events in 18S rRNA 3’ end maturation or metabolism. We quantitatively defined new processing hotspots and identified adenylation as the prevalent non-templated RNA modification at the 3’ ends of pre-18S rRNAs. Aberrant 18S rRNA maturation in hot3 further activated RNAi to generate RDR1- and DCL2/4-dependent risiRNAs mainly from a 3’ portion of 18S rRNA. We further showed that risiRNAs in hot3 were predominantly localized in ribosome-free fractions not responsible for the 18S rRNA maturation or translation initiation defects in hot3. Our study uncovered the molecular function of HOT3/eIF5B1 in 18S rRNA maturation at the late-40S assembly stage and revealed the regulatory crosstalk among ribosome biogenesis, mRNA translation initiation, and siRNA biogenesis in plants.
2023-04-19 | GSE223169 | GEO
Project description:Ribosome biogenesis is essential for protein synthesis in gene expression. Yeast eIF5B has been shown biochemically to facilitate 18S rRNA 3’ end maturation during late-40S ribosomal subunit assembly and gate the transition from translation initiation to elongation. But the effects of eIF5B have not been studied at the genome-wide level in any organism, and 18S rRNA 3’ end maturation is poorly understood in plants. Arabidopsis HOT3/eIF5B1 was found to promote development and heat-stress acclimation by translational regulation, but its molecular function remained unknown. Here, we show that HOT3 is a late-stage ribosome biogenesis factor that facilitates 18S rRNA 3’ end processing and is a translation initiation factor that globally impacts the transition from initiation to elongation. By developing and implementing 18S-ENDseq, we revealed previously unknown events in 18S rRNA 3’ end maturation or metabolism. We quantitatively defined new processing hotspots and identified adenylation as the prevalent non-templated RNA modification at the 3’ ends of pre-18S rRNAs. Aberrant 18S rRNA maturation in hot3 further activated RNAi to generate RDR1- and DCL2/4-dependent risiRNAs mainly from a 3’ portion of 18S rRNA. We further showed that risiRNAs in hot3 were predominantly localized in ribosome-free fractions not responsible for the 18S rRNA maturation or translation initiation defects in hot3. Our study uncovered the molecular function of HOT3/eIF5B1 in 18S rRNA maturation at the late-40S assembly stage and revealed the regulatory crosstalk among ribosome biogenesis, mRNA translation initiation, and siRNA biogenesis in plants.
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Project description:NUP98 rearrangements associated with acute myeloid leukemia and myelodysplastic syndromes generate NUP98-fusion proteins. One such fusion protein, NUP98::DDX10, contains the putative RNA helicase DDX10. The molecular mechanism by which NUP98::DDX10 induces leukemia is not well understood. Here, we show that 24 amino acids within the DDX10 moiety of NUP98::DDX10 are crucial for cell immortalization and leukemogenesis. NOL10, nucleolar protein 10, interacts with the 24 amino acids, and NOL10 is a critical dependency of NUP98::DDX10 leukemia development. Studies in a mouse model of NUP98::DDX10 leukemia showed that loss of Nol10 impaired disease progression and improved survival. We also identified a novel function of NOL10 in that it acts cooperatively with NUP98::DDX10 to regulate serine biosynthesis pathways and stabilize ATF4 mRNA. Collectively, these findings suggest that NOL10 is a critical regulator of NUP98::DDX10 leukemia, and that targeting NOL10 (or the serine synthesis pathway regulated by NOL10) may be an effective therapeutic approach.
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