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Gene expression in Rspo2 and/or Wnt3a treated C57MG mouse mammary epithelial cells

ABSTRACT: R-spondins (Rspos) comprise a family of four secreted proteins that have important roles in cell proliferation, cell fate determination and organogenesis. Rspos typically exert their effects by potentiating the Wnt/β-catenin signaling pathway. To systematically investigate the impact of Rspo/Wnt on gene expression, we performed a microarray analysis using C57MG mouse mammary epithelial cells treated with recombinant Rspo2 and/or Wnt3a.

ORGANISM(S): Mus musculus

PROVIDER: GSE32096 | GEO | 2011/10/05

SECONDARY ACCESSION(S): PRJNA147547

REPOSITORIES: GEO

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Gene expression in Rspo2 and/or Wnt3a treated C57MG mouse mammary epithelial cells

Project description:R-spondins (Rspos) comprise a family of four secreted proteins that have important roles in cell proliferation, cell fate determination and organogenesis. Rspos typically exert their effects by potentiating the Wnt/β-catenin signaling pathway. To systematically investigate the impact of Rspo/Wnt on gene expression, we performed a microarray analysis using C57MG mouse mammary epithelial cells treated with recombinant Rspo2 and/or Wnt3a. This study compares gene expression in C57MG cells after 24h treatment with recombinant Rspo2 and recombinant Wnt3a alone or in combination versus BSA treatment. Control cells were treated with BSA, since it was used as carrier for the recombinant proteins. Each treatment was done in biological triplicate.

2011-10-04 | E-GEOD-32096 | biostudies-arrayexpress

RNA sequencing of WT, TP53KO and onco-RNF43/TP53KO human colon organoid lines.

Project description:RNA sequencing of WT, TP53KO and onco-RNF43/TP53KO human colon organoid lines grown in full medium (high Wnt/Rspo (20%)) or medium without Wnt3a-low Rspo (0.2%).

2020-08-10 | GSE129288 | GEO

KAT6A deficiency impairs cognitive functions through suppressing RSPO2/Wnt signaling in hippocampal CA3 [snRNA-seq]

Project description:Intellectual disability (ID) affects ~2% of the population and ID-associated genes are enriched for epigenetic factors, including those encoding the largest family of histone lysine acetyltransferases (KAT5-KAT8). Among them is KAT6A, whose mutations cause KAT6A Syndrome, with ID as a common clinical feature. However, the underlying molecular mechanism remains unknown. Here, we find that KAT6A deficiency impairs synaptic structure and plasticity in hippocampal CA3, but not in CA1 region, resulting in memory deficits in mice. We further identify a CA3-enriched gene Rspo2, encoding Wnt activator R-spondin 2, as a key transcriptional target of KAT6A. Importantly, deletion of Rspo2 in excitatory neurons impairs memory formation, and restoring RSPO2 expression in CA3 rescues the deficits in Wnt signaling and learning-associated behaviors in Kat6a mutant mice. Collectively, our results demonstrate that KAT6A-RSPO2-Wnt signaling plays a critical role in regulating hippocampal CA3 synaptic plasticity and cognitive function, providing potential therapeutic targets for KAT6A Syndrome and related neurodevelopmental diseases.

2024-03-12 | GSE261148 | GEO

KAT6A deficiency impairs cognitive functions through suppressing RSPO2/Wnt signaling in hippocampal CA3 [RNA-seq]

2024-03-12 | GSE261058 | GEO

R-Spondin chromosome rearrangements drive Wnt-dependent tumor initiation and maintenance in the intestine

Project description:Defining the genetic drivers of cancer progression is key to understanding disease biology and developing effective targeted therapies. Chromosome rearrangements are a common feature of human malignancies, but whether they represent bona fide cancer drivers and therapeutically actionable targets, requires functional testing. Here, we describe the generation of transgenic, inducible CRISPR-based mouse systems to engineer and study recurrent colon cancer-associated EIF3E-RSPO2 and PTPRK-RSPO3 chromosome rearrangements in vivo. We show that both Rspo2 and Rspo3 fusion events are sufficient to initiate hyperplasia and tumor development in vivo, without additional cooperating genetic events. Rspo fusion tumors are entirely Wnt-dependent, as treatment with an inhibitor of Wnt secretion, LGK974, drives rapid tumor clearance from the intestinal mucosa without effects on normal intestinal crypts. Together, our study provides direct evidence that endogenous Rspo2 and Rspo3 chromosome rearrangements can initiate and maintain tumor development, and indicate a viable therapeutic window for LGK974 treatment of RSPO-fusion cancers.

2017-07-01 | GSE98257 | GEO

Transcriptome analysis of the facial processes in Rspo2, WNT9b and Rspo2;Wnt9b double mutant mice

Project description:Purpose: To determine transcriptome profile of the facial processes of Wnt9b, Rspo2 and double gene knockout embryos by NG RNA sequencing Method: Embryonic facial process RNA samples isolated from wild type, Rspo2, Wnt9b and Rspo2;Wnt9b double mutants in triplicate (except wild type (n=2)) at embryonic day 10.5 Results: single-end 50bp reads, 19.8 million reads - 30.7 million reads.

2020-03-25 | GSE147474 | GEO

Transcriptome analysis of Wnt3a-treated triple-negative breast cancer cell lines.

Project description:We analyzed the transcriptome of two different triple negative breast cancer (TNBC) cell lines to define a comprehensive list of Wnt target genes. Cells were treated with Wnt3a for 6h, 12h or 24h. We found up-regulated and down-regulated genes in response to Wnt3a treatment. They are involved in the Wnt pathway itself, and also in TGFM-CM-^_, p53 and Hedgehog pathways. Thorough characterization of these novel potential Wnt target genes may reveal new regulators of the canonical Wnt pathway. The comparison of our list of Wnt target genes with those published in other cellular contexts confirms the notion that Wnt target genes are tissue-, cell line- and treatment-specific. Cells were seeded in six-well plates, serum starved overnight then treated with Wnt3a for the indicated times (6, 12 and 24 hours). Triplicates for each condition were included in the experiment.

2015-01-24 | E-GEOD-65238 | biostudies-arrayexpress

Transcriptome analysis of Wnt3a-treated triple-negative breast cancer cell lines.

Project description:We analyzed the transcriptome of two different triple negative breast cancer (TNBC) cell lines to define a comprehensive list of Wnt target genes. Cells were treated with Wnt3a for 6h, 12h or 24h. We found up-regulated and down-regulated genes in response to Wnt3a treatment. They are involved in the Wnt pathway itself, and also in TGFß, p53 and Hedgehog pathways. Thorough characterization of these novel potential Wnt target genes may reveal new regulators of the canonical Wnt pathway. The comparison of our list of Wnt target genes with those published in other cellular contexts confirms the notion that Wnt target genes are tissue-, cell line- and treatment-specific.

2015-01-24 | GSE65238 | GEO

Expression data from human mesenchymal stem cells treated with Wnt3a

Project description:Wnt signaling is upregulated frequently in several cancers, including sarcomas. Since, there is cell-context dependent variation in the target gene expression, to identify canonical Wnt targets in sarcomas, we used human mesenchymal stem cells. Human mesenchymal stem cells were treated with 100ng/ml recombinant Wnt3a either 6 hrs or 24 hrs. Total RNA was extracted from untreated and Wnt3a treated samples using Qiagen's RNA extraction kit.

2011-02-16 | E-GEOD-27313 | biostudies-arrayexpress

EH004: Lmx1a encodes a rostral set of mesodiencephalic dopaminergic neurons marked by the Wnt/b-catenin signaling activator Rspo2

Project description:Recent developments in molecular programming of mesodiencephalic dopaminergic (mdDA) neurons have led to the identification of many transcription factors playing a role in mdDA specification. LIM homeodomain transcription factor Lmx1a is essential for chick mdDA development, and for the efficient differentiation of ES-cells towards a dopaminergic phenotype. In this study, we aimed towards a more detailed understanding of the subtle phenotype in Lmx1a-dr/dr mice. Therefore, microarray analysis was performed, to elucidate the exact molecular programming underlying the neuronal deficits after loss of Lmx1a. Subsequent expression analysis confirmed that Nurr1 is regulated by Lmx1a, and additional downstream targets were identified, like Pou4f1, Pbx1, Pitx2, C130021l20Rik, Calb2 and Rspo2. In line with a specific, rostral-lateral loss of expression of most of these genes during development, Nurr1 and C130021l20Rik were affected in the SNc of the mature mdDA system. Interestingly, this deficit was marked by the complete loss of the Wnt/b-catenin signaling activator Rspo2 in this domain. Expression analysis in Rspo2-/- embryos revealed affected mdDA neurons, partially phenocopying the Lmx1a mutant. Together, in this study we reveal that Lmx1a is essential for a rostral-lateral subset of the mdDA neuronal field, where it might serve a critical function in modulating proliferation and differentiation of mdDA progenitors through the activation of the Wnt activator Rspo2. Microarray expression study comparing 4 samples of homozygous LMX1A dr/dr mice, midbrain E12.5 with a pooled sample of their wt/wt littermates. Two samples were analyzed in opposite dye orientation.

2013-12-13 | E-GEOD-45831 | biostudies-arrayexpress

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