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Sex-dependent gene expression patterns in control and Rspo1 gain-of-function mouse adrenals

ABSTRACT: Sex-dependent gene expression patterns in control and Rspo1 gain-of-function mouse adrenals

PROVIDER: PRJNA741670 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14919971_1.fastq.gz	Fastqsanger.gz
	SRR14919971_2.fastq.gz	Fastqsanger.gz
	SRR14919972_1.fastq.gz	Fastqsanger.gz
	SRR14919972_2.fastq.gz	Fastqsanger.gz
	SRR14919973_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Sex-dependent gene expression patterns in control and Rspo1 gain-of-function mouse adrenals

Project description:Purpose: Ectopic Rspo1 expression in the mouse adrenal gland (driven by Sf1-Cre) leads to a sexually dimorphic phenotype of adrenocortical hyperplasia and tissue degeneration. In order to gain a mechanistic understanding of the sexual dimorphism, we compared the gene expression profiles of Rspo1-overexpressing animals (Rspo1 GOF) with control littermates. Methods: Total RNA was extracted from whole adrenals of male and female, control and Rspo1GOF mice during puberty (4 weeks). mRNA sequencing and differential gene expression analysis was conducted by Novogene Co. Hierarchical clustering and principal component analysis were conducted using Phantasus. Gene set enrichment analysis was performed using Broad's institute GSEA and the Molecular Signatures database. Conclusions: After Rspo1 transgene expression, sex is the second most important component that explains variability among the experimental groups. Genes specifically upregulated in female Rspo1GOF adrenals vs all the other groups are enriched in DNA proliferation and cell cycle genes, targets of E2F transcription factros and the DREAM complex. Genes specifically upregulated in male Rspo1GOF adrenals are related to immune system regulation. Verification of the RNA Seq results by experimental methods has showed that ectopic proliferation in the mutant adrenals is female-specific and that androgen receptor signalling plays a role in proliferation arrest in male animals. Moreover, accumulation of abnormal foamy-like macrophages in the male adrenals leads to tissue degeneration.

2021-06-27 | GSE178958 | GEO

Rspo1 role in mammary gland during pregnancy

Project description:R-spondin1 (Rspo1) is a member of a secreted protein family which has pleiotropic functions in development and stem cell growth. Rspo1 knock-out mice are sex-reversed, but some remain sub-fertile, so, they are unable to nurse their pups. A lack of Rspo1 expression in mammary epithelial cells results in an absence of duct side-branching development and defective alveolar formation. In this study we propose to characterize the molecular functions involved to mammary gland phenotype due to Rspo1 knock out. By transcriptional profiling, we have identified gene misregulated in mammary gland of Rspo1 knock-out mice during pregnancy. A stronger expression of genes characterising mesenchymal tissue was observed in the absence of alterations to the structure of mammary epithelial tissue. Mammary epithelial cell characterization, by immunohistochemistry approach, revealed a persistence of virgin markers which sign a delay in their differentiation. Moreover serial transplantation experiments show that Rspo1 is associated with a regenerative potential of mammary epithelial cell control. Our data have also highlighted that in mammary gland during pregnancy the expression of Rspo1’s partners, Lgr4 and RNF43, are negatively regulated and Tgf-β signaling is modified in the absence of Rspo1. Taken together, our results show an abrupt halt in mammary development at mid-pregnancy due to loss of further differentiated function.

2017-02-09 | GSE81244 | GEO

Sex and mutation specific p53 gain-of-function activity in gliomagenesis

Project description:Sex and mutation specific p53 gain-of-function activity in gliomagenesis

| PRJNA779976 | ENA

RNA-seq analysis of FET cells treated with RSPO1 or TGFβ1

Project description:To determine whether RSPO1 and TGFβ1 activate similar transcription, RNA-seq analysis was performed to compare gene profiles after treatment by RSPO1 or TGFβ1. FET cells were treated with RSPO1 or TGFβ1 in triplicates for 4 hours and RNAs extracted from these cells were used for RNA-seq analysis. When gene expression profiles were compared, it was found that 153 genes were commonly regulated by either RSPO1 or TGFβ1. Interestingly, the majority of genes regulated by TGFβ1 were also regulated by RSPO1.

2017-09-09 | GSE103650 | GEO

Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

Project description:The goal of this study is to compare the sex specific effects of the expression of p53 missense mutations on the transcriptomes of male and female primary astrocytes. Primary cortical astrocytes harboring a single floxed Trp53 allele were harvested from male and female postnatal day one pups, and transduced with mutant p53;IRES GFP followed by CRE recombinase. mRNA was collected from male and female astrocytes transduce with mouse Trp53:R172H, Trp53:Y202C, or Trp53:Y217C. This study revealed sex specific gain-of-function effects on the transcriptomes of each cell line that correlated with cancer pathways.

2021-11-16 | GSE188709 | GEO

Single cell changes in RSPO1-Fc treated intestinal adenoma organoids from ApcMin/+ mice

Project description:We constructed AAV-vectors for systemic expression of a soluble RSPO1 protein in ApcMin/+ mice. We found that the RSPO1-Fc fusion protein suppresses the Wnt/ß-catenin signaling activity in intestinal adenomas and in adenoma-derived intestinal organoids ex vivo, but not in normal intestinal epithelial cells. In the Apc mutant cells, the RSPO1-Fc fusion protein activated the TGFß/SMAD signaling pathway to suppress several Wnt target genes and adenoma growth, which effect was rescued suppressed by the TGFß receptor kinase inhibitor SB-431542. Simultaneously, RSPO1-Fc induced proliferation of the normal intestinal stem cells, giving them a growth advantage over the mutant cells, which enabled the intestinal epithelium to eventually outgrow the adenoma cells. Prolonged systemic expression of AAV-RSPO1-Fc decreased significantly the number of the intestinal adenomas and improved the overall survival of ApcMin/+ mice. Thus RSPO1-Fc provides the normal intestinal epithelial cells a growth advantage when compared to the adenoma cells, which eventually leads to the extrusion of the adenomatous tissue. An attractive idea now is to exploit such differential response of normal vs. cancer cells in cancer therapy.

2020-02-29 | GSE146099 | GEO

Sex and mutation specific p53 gain-of-function activity in gliomagenesis [ChIP-seq]

Project description:Sex and mutation specific p53 gain-of-function activity in gliomagenesis [ChIP-seq]

| PRJNA779981 | ENA

Sex-specific roles of PKLR in NAFLD using gain-of-function mouse models

Project description:Sex-specific roles of PKLR in NAFLD using gain-of-function mouse models

| PRJNA660435 | ENA

Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

Project description:Sex and mutation specific p53 gain-of-function activity in gliomagenesis [RNA-seq]

| PRJNA779980 | ENA

RNAseq of Axin2pos and Axin2neg cell populations derived from differentiated bile duct organoids treated with Rspo1

Project description:Purpose: The goal of this study was to compare the transcriptome profiling (RNAseq) of two cell populations (Axin2pos and Axin2neg) that in differentiated bile duct-derived organoids (Axin2CreERT2+/-; R26-LSL-tdTom+/-) that aroused following 24h Rspo1 treatment. The transcriptome of these two cell populations was additionally compared with cells isolated from differentiated control organoids, which were all negative for Axin2 expression. Methods: Single-end 75bp sequencing of Axin2pos and Axin2neg cells isolated by FACS from differentiated bile duct organoids (Axin2CreERT2+/-; R26-LSL-tdTom+/-) organoids at three different passages (P5, P6 and P10) based on tdTom expression levels was performed with 100ng of total RNA input. To label Axin2 expressing cells, organoids treated with 500nM of 4-OHT for the last 24h of culture. Rspo1-treated organoids were exposed to 100ng/ml of Rspo1 during the last 24h of culture. Results: The addition of Rspo1 to the cultures caused an overall decrease of BEC lineage markers (Hnf1b, Muc1, Krt19, Krt7) in both Axin2pos and Axin2neg cells when compared to untreated cells, indicating that exposure to Rspo1 promoted escape from biliary fate. Axin2pos isolated from Rspo1-treated organoids were enriched in proliferation and hepatic progenitor cell markers when compared to Axin2neg cells isolated from Rspo1 treated organoids Conclusions: Our study uncover a possible role for the Wnt signalling pathway in BEC regenerative biology and cellular plasticity.

2020-11-09 | GSE161039 | GEO

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