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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Danio rerio

PROVIDER: GSE191003 | GEO | 2021/12/17

REPOSITORIES: GEO

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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 [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: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: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 [bulk RNA-seq]

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

| PRJNA789278 | ENA

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

Ribosomal biogenesis genes play an essential and p53-independent role in zebrafish pancreas development.

Project description:Mutations in the human Shwachman-Bodian-Diamond syndrome (SBDS) gene cause defective ribosome assembly and are associated with exocrine pancreatic insufficiency, chronic neutropenia and skeletal defects. However, the mechanism underlying these phenotypes remains unclear. Here we show that knockdown of the zebrafish sbds ortholog fully recapitulates the spectrum of developmental abnormalities observed in the human syndrome, and further implicate impaired proliferation of ptf1a-expressing pancreatic progenitor cells as the basis for the observed pancreatic phenotype. It is thought that diseases of ribosome assembly share a p53-dependent mechanism. However, loss of p53 did not rescue the developmental defects associated with loss of zebrafish sbds. To clarify the molecular mechanisms underlying the observed organogenesis defects, we performed transcriptional profiling to identify candidate downstream mediators of the sbds phenotype. Among transcripts displaying differential expression, functional group analysis revealed marked enrichment of genes related to ribosome biogenesis, rRNA processing and translational initiation. Among these, ribosomal protein L3 (rpl3) and pescadillo (pes) were selected for additional analysis. Similar to knockdown of sbds, knockdown or mutation of either rpl3 or pes resulted in impaired expansion of pancreatic progenitor cells. The pancreatic phenotypes observed in rpl3- and pes-deficient embryos were also independent of p53. Together, these data suggest novel p53-independent roles for ribosomal biogenesis genes in zebrafish pancreas development.

| S-EPMC3413166 | biostudies-literature

Impaired neural development in a zebrafish model for Lowe syndrome.

Project description:Lowe syndrome, which is characterized by defects in the central nervous system, eyes and kidneys, is caused by mutation of the phosphoinositide 5-phosphatase OCRL1. The mechanisms by which loss of OCRL1 leads to the phenotypic manifestations of Lowe syndrome are currently unclear, in part, owing to the lack of an animal model that recapitulates the disease phenotype. Here, we describe a zebrafish model for Lowe syndrome using stable and transient suppression of OCRL1 expression. Deficiency of OCRL1, which is enriched in the brain, leads to neurological defects similar to those reported in Lowe syndrome patients, namely increased susceptibility to heat-induced seizures and cystic brain lesions. In OCRL1-deficient embryos, Akt signalling is reduced and there is both increased apoptosis and reduced proliferation, most strikingly in the neural tissue. Rescue experiments indicate that catalytic activity and binding to the vesicle coat protein clathrin are essential for OCRL1 function in these processes. Our results indicate a novel role for OCRL1 in neural development, and support a model whereby dysregulation of phosphoinositide metabolism and clathrin-mediated membrane traffic leads to the neurological symptoms of Lowe syndrome.

| S-EPMC3313792 | biostudies-literature

Pcgf1 Regulates Early Neural Tube Development Through Histone Methylation in Zebrafish.

Project description:The neural induction constitutes the initial step in the generation of the neural tube. Pcgf1, as one of six Pcgf paralogs, is a maternally expressed gene, but its role and mechanism in early neural induction during neural tube development have not yet been explored. In this study, we found that zebrafish embryos exhibited a small head and reduced or even absence of telencephalon after inhibiting the expression of Pcgf1. Moreover, the neural induction process of zebrafish embryos was abnormally activated, and the subsequent NSC self-renewal was inhibited after injecting the Pcgf1 MO. The results of in vitro also showed that knockdown of Pcgf1 increased the expression levels of the neural markers Pax6, Pou3f1, and Zfp521, but decreased the expression levels of the pluripotent markers Oct4, Hes1, and Nanog, which further confirmed that Pcgf1 was indispensable for maintaining the pluripotency of P19 cells. To gain a better understanding of the role of Pcgf1 in early development, we analyzed mRNA profiles from Pcgf1-deficient P19 cells using RNA-seq. We found that the differentially expressed genes were enriched in many functional categories, which related to the development phenotype, and knockdown of Pcgf1 increased the expression of histone demethylases. Finally, our results showed that Pcgf1 loss-of-function decreased the levels of transcriptional repression mark H3K27me3 at the promoters of Ngn1 and Otx2, and the levels of transcriptional activation mark H3K4me3 at the promoters of Pou5f3 and Nanog. Together, our findings reveal that Pcgf1 might function as both a facilitator for pluripotent maintenance and a repressor for neural induction.

| S-EPMC7870693 | biostudies-literature

Loss of ribosomal protein L11 affects zebrafish embryonic development through a p53-dependent apoptotic response.

Project description:Ribosome is responsible for protein synthesis in all organisms and ribosomal proteins (RPs) play important roles in the formation of a functional ribosome. L11 was recently shown to regulate p53 activity through a direct binding with MDM2 and abrogating the MDM2-induced p53 degradation in response to ribosomal stress. However, the studies were performed in cell lines and the significance of this tumor suppressor function of L11 has yet to be explored in animal models. To investigate the effects of the deletion of L11 and its physiological relevance to p53 activity, we knocked down the rpl11 gene in zebrafish and analyzed the p53 response. Contrary to the cell line-based results, our data indicate that an L11 deficiency in a model organism activates the p53 pathway. The L11-deficient embryos (morphants) displayed developmental abnormalities primarily in the brain, leading to embryonic lethality within 6-7 days post fertilization. Extensive apoptosis was observed in the head region of the morphants, thus correlating the morphological defects with apparent cell death. A decrease in total abundance of genes involved in neural patterning of the brain was observed in the morphants, suggesting a reduction in neural progenitor cells. Upregulation of the genes involved in the p53 pathway were observed in the morphants. Simultaneous knockdown of the p53 gene rescued the developmental defects and apoptosis in the morphants. These results suggest that ribosomal dysfunction due to the loss of L11 activates a p53-dependent checkpoint response to prevent improper embryonic development.

| S-EPMC2612748 | biostudies-literature

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