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MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with Host Cell Factor-1

ABSTRACT: MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with Host Cell Factor-1

PROVIDER: PRJNA639148 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12005244_1.fastq.gz	Fastqsanger.gz
	SRR12005244_2.fastq.gz	Fastqsanger.gz
	SRR12005245_1.fastq.gz	Fastqsanger.gz
	SRR12005245_2.fastq.gz	Fastqsanger.gz
	SRR12005246_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with Host Cell Factor-1

Project description:MYC is an oncoprotein transcription factor that is overexpressed in the majority cancers. Although MYC itself is considered undruggable, it may be possible to inhibit MYC by targeting the co-factors it uses to drive oncogenic gene expression patterns. Here, we use loss- and gain- of function approaches to interrogate how one MYC co-factor—Host Cell Factor (HCF)-1—contributes to MYC activity in a Burkitt lymphoma setting. We identify high-confidence direct targets of the MYC–HCF-1 interaction that are regulated through a recruitment-independent mechanism, including genes that control mitochondrial function and rate-limiting steps for ribosome biogenesis and translation. We describe how these gene expression events impact cell growth and metabolism, and demonstrate that the MYC–HCF-1 interaction is essential for tumor maintenance in vivo. This work highlights the MYC–HCF-1 interaction as a focal point for development of novel anti-cancer therapies.

2020-07-15 | ST001429 | MetabolomicsWorkbench

MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with Host Cell Factor-1

2021-01-11 | GSE152385 | GEO

GNPS Metabolomics Workbench ST001429 - GNPS MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with Host Cell Factor-1

Project description:b'MYC is an oncoprotein transcription factor that is overexpressed in the majority cancers. Although MYC itself is considered undruggable, it may be possible to inhibit MYC by targeting the co-factors it uses to drive oncogenic gene expression patterns. Here, we use loss- and gain- of function approaches to interrogate how one MYC co-factorHost Cell Factor (HCF)-1contributes to MYC activity in a Burkitt lymphoma setting. We identify high-confidence direct targets of the MYCHCF-1 interaction that are regulated through a recruitment-independent mechanism, including genes that control mitochondrial function and rate-limiting steps for ribosome biogenesis and translation. We describe how these gene expression events impact cell growth and metabolism, and demonstrate that the MYCHCF-1 interaction is essential for tumor maintenance in vivo. This work highlights the MYCHCF-1 interaction as a focal point for development of novel anti-cancer therapies.'

2021-02-17 | MSV000086896 | GNPS

MYC regulates ribosome biogenesis and mitochondrial gene expression programs through its interaction with host cell factor-1.

Project description:The oncoprotein transcription factor MYC is a major driver of malignancy and a highly validated but challenging target for the development of anticancer therapies. Novel strategies to inhibit MYC may come from understanding the co-factors it uses to drive pro-tumorigenic gene expression programs, providing their role in MYC activity is understood. Here we interrogate how one MYC co-factor, host cell factor (HCF)-1, contributes to MYC activity in a human Burkitt lymphoma setting. We identify genes connected to mitochondrial function and ribosome biogenesis as direct MYC/HCF-1 targets and demonstrate how modulation of the MYC-HCF-1 interaction influences cell growth, metabolite profiles, global gene expression patterns, and tumor growth in vivo. This work defines HCF-1 as a critical MYC co-factor, places the MYC-HCF-1 interaction in biological context, and highlights HCF-1 as a focal point for development of novel anti-MYC therapies.

| S-EPMC7793627 | 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

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.

| PRJNA761360 | ENA

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

Post-transcriptional regulation of Ribosome Biogenesis

Project description:Post-transcriptional regulation of Ribosome Biogenesis

| PRJNA970342 | ENA

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

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