LncRNAs regulate FBL to facilitate rRNA processing in cancer cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1155179 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30504235.fastq.gz | Fastqsanger.gz | |||
| SRR30504236.fastq.gz | Fastqsanger.gz | |||
| SRR30504237.fastq.gz | Fastqsanger.gz | |||
| SRR30504238.fastq.gz | Fastqsanger.gz | |||
| SRR30504239.fastq.gz | Fastqsanger.gz |
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Project description:We identified lncRNA DNAJC3-AS1 can buffer the behavior of FBL condensation in cancer cell. In this study, we preformed the FBL-TurboID-RIP and Single-end Enhanced Cross-linking and Immunoprecipitation (seCLIP) sequencing to to identify candidate RNAs that bind to FBL or its adjacent proteins. The FBL-binding regions distributed throughout the sequence of lncRNAs were also discovered.
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Project description:Pluripotent stem cells have been shown to have unique nuclear properties, e.g., hyperdynamic chromatin and large, condensed nucleoli. However, the contribution of the latter unique nucleolar character to pluripotency has not been well understood. Here, we show fibrillarin (FBL), a critical methyltransferase for ribosomal RNA (rRNA) processing in nucleoli, as one of the proteins highly expressed in pluripotent embryonic stem (ES) cells. Stable expression of FBL in ES cells prolonged the pluripotent state of mouse ES cells cultured in the absence of leukemia inhibitory factor (LIF). Analyses using deletion mutants and a point mutant revealed that the methyltransferase activity of FBL regulates stem cell pluripotency. Knock down of this gene led to significant delays in rRNA processing, growth inhibition, and apoptosis in mouse ES cells. Interestingly, both partial knock down of FBL and treatment with actinomycin D, an inhibitor for rRNA synthesis, induced the expression of differentiation markers in the presence of LIF and promoted stem cell differentiation into neuronal lineages. Moreover, we identified p53 signaling as the regulatory pathway for pluripotency and differentiation of ES cells. These results suggest that proper activity of rRNA production in nucleoli is a novel factor for the regulation of pluripotency and differentiation ability of ES cells. Tc-inducible FBL-knock down ES cells were cultured for 2 days with or without Tc in the presence of LIF. These 2 conditions were analysed transcription profile.
2014-08-01 | E-GEOD-51139 | biostudies-arrayexpress
Project description:Pluripotent stem cells have been shown to have unique nuclear properties, e.g., hyperdynamic chromatin and large, condensed nucleoli. However, the contribution of the latter unique nucleolar character to pluripotency has not been well understood. Here, we show fibrillarin (FBL), a critical methyltransferase for ribosomal RNA (rRNA) processing in nucleoli, as one of the proteins highly expressed in pluripotent embryonic stem (ES) cells. Stable expression of FBL in ES cells prolonged the pluripotent state of mouse ES cells cultured in the absence of leukemia inhibitory factor (LIF). Analyses using deletion mutants and a point mutant revealed that the methyltransferase activity of FBL regulates stem cell pluripotency. Knock down of this gene led to significant delays in rRNA processing, growth inhibition, and apoptosis in mouse ES cells. Interestingly, both partial knock down of FBL and treatment with actinomycin D, an inhibitor for rRNA synthesis, induced the expression of differentiation markers in the presence of LIF and promoted stem cell differentiation into neuronal lineages. Moreover, we identified p53 signaling as the regulatory pathway for pluripotency and differentiation of ES cells. These results suggest that proper activity of rRNA production in nucleoli is a novel factor for the regulation of pluripotency and differentiation ability of ES cells.
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Project description:We performed CLASH for 15.5K and FBL in HEK293T cells which overexpressed 15.5K and FBL, respectively.
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Project description:Ribosomal RNAs (rRNAs) are main effectors of mRNA decoding, peptide-bond formation and ribosome dynamics during translation. Ribose 2'-O-methylation is the most abundant rRNA chemical modification, and display a complex pattern in rRNA. We globally challenged rRNA 2'-O-Me by inhibiting the rRNA methyl-transferase fibrillarin (FBL) in human cells. Since FBL participates in rRNA processing, we wonder if FBL knockdown could alter the assembly of ribosomes.
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Project description:Exploring the mechanism of transformation and propagation of acute myeloid leukemia is still the key to solving its refractory and relapse-prone problems. Phase separation refers to the process of specific aggregation of biological macromolecules through multivalent binding, and then leads to the functional sectorization in cell. Despite the fact that phase separation has been related to the dysregulation of various cellular processes, its role in the malignant transformation and development of AML is still less characterized. Nucleolus, as a multilayer condensate formed by phase separation, is an important place for the initiation of ribosome formation, and its function is directly related to protein translation.High-resolution imaging and fluorescence recovery after photo-bleaching experiments decode the positive regulatory relationship between the phase separation of FBL and the structure and function of nucleoli. Here, we used RiboMeth-seq to examine rRNA 2’-O-me modification changes influenced by FBL knockdown in AML cells.
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Project description:In order to study the molecular mechanism of FBL in cells, this project constructed the full length of FBL into the SFB (S-Flag-SBP tag) vector, and constructed a stable cell line overexpressing FBL. Affinity chromatography combined with LC-MS/MS technology to screen FBL interacting proteins.
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Project description:2′-O-Methylation is prominent in ribosome RNA catalyzed by Fibrillarin (FBL). However, the stoichiometry of 2′-O-methylation at base resolution in the internal mRNA and its functions remain to be explored. Here, we firstly investigate the effect of the 2′-O-methylation on the mRNA stability and expression at a genome-wide scale. Combined with Nanopore sequencing and a machine learning strategy, we identified thousands of RNA methylation sites in mRNA and rRNA at base resolution. The mRNA half-life profiling of FBL deficient cells established a direct effect of RNA methylation and FBL binding on the mRNA stability. We further determined the RNA methylation on the expression levels and tested the post-transcriptional effect of elevated FBL mediated 2′-O-Methylation in mRNA within the prostate cancer model. Besides the role of the translational regulation of FBL in rRNA, elevated FBL promotes cancer progress by stabilizing the mRNA through RNA binding and 2′-O-Methylation. Our results reveal a novel mechanism that FBL regulates the 2′-O-methylation and turnover of mRNA at whole transcriptome levels.
2024-06-20 | GSE208837 | GEO
Project description:Overactivated ribosome biogenesis is a common feature of cancer. However, the underlying molecular mechanism remains elusive. Herein, we report enhancer of zeste homolog 2 (EZH2), a histone methyltransferase, could interact with fibrillarin (FBL) directly in the nucleolus. While loss of EZH2 does not impact FBL-mediated histone H2AQ104 methylation (H2AQ104me) and 18S rRNA processing, EZH2 is proved to be involved in rRNA 2′-O methylation in a manner dependent of its interaction with FBL. Mechanistically, EZH2 strengthens the fibrillarin (FBL)-NOP56 interaction by binding to both proteins and thus facilitates the assembly of box C/D small nucleolar ribonucleoprotein (box C/D snoRNP). Strikingly, EZH2 deficiency alters translational efficiency and reduces internal ribosome entry site (IRES) activity of key oncogenes in prostate cancer. In summary, our findings reveal a novel non-methyltransferase role of EZH2 that mediates FBL functions, which may provide more options for the development of EZH2-targeting curative strategies in cancer.
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Project description:Overactivated ribosome biogenesis is a common feature of cancer. However, the underlying molecular mechanism remains elusive. Herein, we report enhancer of zeste homolog 2 (EZH2), a histone methyltransferase, could interact with fibrillarin (FBL) directly in the nucleolus. While loss of EZH2 does not impact FBL-mediated histone H2AQ104 methylation (H2AQ104me) and 18S rRNA processing, EZH2 is proved to be involved in rRNA 2′-O methylation in a manner dependent of its interaction with FBL. Mechanistically, EZH2 strengthens the fibrillarin (FBL)-NOP56 interaction by binding to both proteins and thus facilitates the assembly of box C/D small nucleolar ribonucleoprotein (box C/D snoRNP). Strikingly, EZH2 deficiency alters translational efficiency and reduces internal ribosome entry site (IRES) activity of key oncogenes in prostate cancer. In summary, our findings reveal a novel non-methyltransferase role of EZH2 that mediates FBL functions, which may provide more options for the development of EZH2-targeting curative strategies in cancer.
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