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Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1 [bulk RNA-seq]

ABSTRACT: Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1 [bulk RNA-seq]

PROVIDER: PRJNA789278 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17239186_1.fastq.gz	Fastqsanger.gz
	SRR17239186_2.fastq.gz	Fastqsanger.gz
	SRR17239187_1.fastq.gz	Fastqsanger.gz
	SRR17239187_2.fastq.gz	Fastqsanger.gz
	SRR17239188_1.fastq.gz	Fastqsanger.gz

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Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1 [bulk RNA-seq]

Project description:Purpose: To identify differential expressed genes for loss of function of Mycn in zebrafish Methods: wild-type and mycn mutant zebrafish embryos were collected for RNA sequencing at 48 hpf (hours post fertilisation) and 72 hpf Results: We found 85 (overlapped) down-regulated genes in mycn mutant embryos at 48 hpf and 72 hpf (padj < 0.1, log2 fold change < 0) Conclusions: 85 down-regulated genes were identified

2021-12-17 | GSE191001 | GEO

Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1

Project description:Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1

| PRJNA789272 | ENA

Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1 (RNA-seq and Ribo-seq)

Project description:Purpose: To systematically investigate the molecular mechanisms resulting from Mycn loss-of-function. Methods: Approximately 30 mycn mutant or WT zebrafish embryos at 72 hpf (hours post fertilization) were harvested . Libraries were prepared using Chromium Controller and Chromium Single Cell 3’Library & Gel Bead Kit v3 (10x Genomics, PN-1000074) according to the manufacturer’s protocol for 10000 cells recovery. Results: More than 3,000 genes showed reduced tranlation efficiency in Mycn mutant. Conclusions: mTOR signaling was reduced in Mycn mutant.

2022-08-26 | GSE211652 | GEO

Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1.

Project description:Feingold syndrome type 1, caused by loss-of-function of MYCN, is characterized by varied phenotypes including esophageal and duodenal atresia. However, no adequate model exists for studying the syndrome's pathological or molecular mechanisms, nor is there a treatment strategy. Here, we developed a zebrafish Feingold syndrome type 1 model with nonfunctional mycn, which had severe intestinal atresia. Single-cell RNA-seq identified a subcluster of intestinal cells that were highly sensitive to Mycn, and impaired cell proliferation decreased the overall number of intestinal cells in the mycn mutant fish. Bulk RNA-seq and metabolomic analysis showed that expression of ribosomal genes was down-regulated and that amino acid metabolism was abnormal. Northern blot and ribosomal profiling analysis showed abnormal rRNA processing and decreases in free 40S, 60S, and 80S ribosome particles, which led to impaired translation in the mutant. Besides, both Ribo-seq and western blot analysis showed that mTOR pathway was impaired in mycn mutant, and blocking mTOR pathway by rapamycin treatment can mimic the intestinal defect, and both L-leucine and Rheb, which can elevate translation via activating TOR pathway, could rescue the intestinal phenotype of mycn mutant. In summary, by this zebrafish Feingold syndrome type 1 model, we found that disturbance of ribosomal biogenesis and blockage of protein synthesis during development are primary causes of the intestinal defect in Feingold syndrome type 1. Importantly, our work suggests that leucine supplementation may be a feasible and easy treatment option for this disease.

| S-EPMC9624419 | biostudies-literature

Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1 [single-cell RNA-seq]

Project description:Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1 [single-cell RNA-seq]

| PRJNA789277 | ENA

Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1 [single-cell RNA-seq]

Project description:Purpose: To systematically investigate the phenotypes resulting from Mycn loss-of-function at a higher resolution. Methods: Approximately 30 mycn mutant or WT zebrafish embryos at 72 hpf (hours post fertilization) were harvested . Libraries were prepared using Chromium Controller and Chromium Single Cell 3’Library & Gel Bead Kit v3 (10x Genomics, PN-1000074) according to the manufacturer’s protocol for 10000 cells recovery. Results: A total of 25,886 single-cell transcriptomes were collected after stringent quality control measures. Conclusions: 27 Cell types were identified by intergrating two datasets and 9 subclusters were obtained by reclustering intestinal cells.

2021-12-17 | GSE191002 | GEO

Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1 (RNA-seq and Ribo-seq)

Project description:Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1 (RNA-seq and Ribo-seq)

| PRJNA871254 | ENA

Mycn regulates intestinal development through ribosomal biogenesis in a zebrafish model of Feingold syndrome 1

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

2021-12-17 | GSE191003 | GEO

LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RNA-Seq)

Project description:High expression of LIN28B is associated with aggressive malignancy and poor survival. Here, probing MYCN-amplified neuroblastoma as a model system, we show that LIN28B expression is associated with enhanced cell migration in vitro and invasive and metastatic behavior in murine xenografts. Sequence analysis of the polyribosome fraction of LIN28B-expressing neuroblastoma cells revealed let-7 independent enrichment of transcripts encoding components of the translational and ribosomal apparatus, particularly those with higher Adenine/Uridine (AU)-content, and depletion of GC-rich transcripts of neuronal developmental programs. We further show that LIN28B utilizes both its cold shock and zinc finger RNA binding domains to preferentially interact with MYCN-induced transcripts of the ribosomal complex, enhancing their translation. These data demonstrate that LIN28B couples the MYCN-driven transcriptional program to enhanced ribosomal translation, thereby implicating LIN28B as a post-transcriptional driver of the metastatic phenotype.

2022-09-30 | GSE158320 | GEO

LIN28B alters ribosomal dynamics to promote metastasis in MYCN-driven malignancy (RIP-Seq)

Project description:High expression of LIN28B is associated with aggressive malignancy and poor survival. Here, probing MYCN-amplified neuroblastoma as a model system, we show that LIN28B expression is associated with enhanced cell migration in vitro and invasive and metastatic behavior in murine xenografts. Sequence analysis of the polyribosome fraction of LIN28B-expressing neuroblastoma cells revealed let-7 independent enrichment of transcripts encoding components of the translational and ribosomal apparatus, particularly those with higher adenine/uridine (AU)-content, and depletion of transcripts of neuronal developmental programs. We further show that LIN28B utilizes both its cold shock and zinc finger RNA binding domains to preferentially interact with MYCN-induced transcripts of the ribosomal complex, enhancing their translation. These data demonstrate that LIN28B couples the MYCN-driven transcriptional program to enhanced ribosomal translation, thereby implicating LIN28B as a post-transcriptional driver of the metastatic phenotype.

2022-09-30 | GSE183336 | GEO

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