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Effect of inactivation of Mst1 and Mst2 in the mouse adrenal cortex

ABSTRACT: The Hippo Pathway has been found to play an important role in adrenal gland development and maintenance in mice. In this study, we further explored the role of the Hippo pathway in the adrenal gland using a transgenic mouse model where we knocked out the upstream kinases of the pathway, Mst1 and Mst2.

ORGANISM(S): Mus musculus

PROVIDER: GSE185401 | GEO | 2022/09/14

REPOSITORIES: GEO

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Microarray of Mst1/2 deleted epithelial cells from E18.5 mouse lungs

Project description:ShhCre;Mst1/2flx/flx (Mst1/2 D/D) mice were generated to conditionally delete Mst1 and Mst2 from epithelial progenitors during lung morphogenesis. Lungs from E18.5 control and Mst1/2 D/D mice were mechanically and enzymatically dissociated to generate single cell suspension. Epcam(+) cells were isolated using magnetic microbeads. Microarray analysis of mRNAs isolated from Epcam(+) epithelial cells from E18.5 control and Mst1/2 D/D mice was performed to identify transcriptional changes following deletion of the mammalian Hippo kinases (Mst1 and Mst2) from the embryonic lung. The mammalian Hippo kinases, Mst1 and Mst2, were conditionally deleted in epithelial progenitors of the developing lung using ShhCre. Epcam(+) epithelial cells were isolated from the lungs of E18.5 control and Mst1/2 deleted mice. mRNA isolated from Epcam(+) epithelial cells was analyzed by microarray.

2015-01-01 | E-GEOD-61582 | biostudies-arrayexpress

RNA sequencing data from wild type and Mst1/2 knockout esophageal epithelium

Project description:Hippo signaling regulates the homeostasis of multiple organs. Mst1 and Mst2 (Mst1/2) are critical components of the Hippo signaling pathway. Here, we utilized RNA sequencing to determine the transcriptional change in the esophageal epithelium upon Mst1/2 deletion. The analysis of gene expression profiles allows us to understand the role of Mst1/2 in the regulation of various biological processes in the esophageal epithelium.

2024-02-26 | GSE248501 | GEO

Expression data from Mst knockout embryoid bodies and wild type embryoid bodies

Project description:Mst1/Mst2 are central components of Hippo pathway. We examined the role of Mst1/Mst2 in ES cell differentiation. In this data set, we include expression data from day 4 and day 8 Mst1/Mst2 knockout ES cell formed embryoid bodies and wild type embryoid body controls. total 4 samples.

2014-01-02 | E-GEOD-50219 | biostudies-arrayexpress

Hippo kinases Mst1 and Mst2 sense and amplify IL-2R−STAT5 signaling in Treg cells to establish stable regulatory activity

Project description:Interleukin-2 (IL-2) and downstream transcription factor STAT5 are important for maintaining regulatory T (Treg) cell homeostasis and function. Tregs can respond to low levels of IL-2, but the mechanisms by which STAT5 is activated during partial IL-2 deficiency remain uncertain. We identified the serine-threonine kinase Mst1 as a signal-dependent amplifier of IL-2−STAT5 activity in Tregs. Tregs had high Mst1 and Mst2 (Mst1−Mst2) activity that was crucial to prevent tumor resistance and autoimmunity. Mechanistically, Mst1−Mst2 sensed IL-2 signals to promote the STAT5 activation necessary for Treg cell homeostasis and lineage stability, and maintain the highly suppressive phophorylated-STAT5+ Treg cell subpopulation. Unbiased quantitative proteomics revealed an association of Mst1 with the cytoskeletal DOCK8−LRCHs module that shaped activity Rho-family GTPase Rac activity, which in turn mediated STAT5 activation in Tregs. Collectively, IL-2−STAT5 signaling critically depends upon Mst1−Mst2 functions to maintain a stable Treg cell pool and immune tolerance. We used microarrays to compare the global transcription profiles of WT and Mst1/Mst2-null Treg cell populations

2018-11-08 | GSE120711 | GEO

Microarray of Mst1/2 deleted epithelial cells from E18.5 mouse lungs

2015-01-01 | GSE61582 | GEO

Expression data from Mst knockout embryoid bodies and wild type embryoid bodies

2014-01-02 | GSE50219 | GEO

Targeted disruption of Mst1 and Mst2 in the mouse adrenal gland causes the remature accumulation of subcapsular adrenal gonadal primordium (AGP)-like progenitor cells

Project description:Targeted disruption of Mst1 and Mst2 in the mouse adrenal gland causes the remature accumulation of subcapsular adrenal gonadal primordium (AGP)-like progenitor cells

| PRJNA768884 | ENA

RNA-seq analysis of Mst1/2 deleted bronchiolar epithelial cells from adult mouse lungs

Project description:Mst1 and Mst2 were conditionally deleted from non-ciliated bronchiolar epithelial cells in the mature lung. Bronchiolar epithelial cells from control and Mst1/2 deleted mice were isolated by cell sorting and used for RNA-seq analysis. Scgb1a1-rtTA/tetO-Cre/Mst1;2-flx/flx (Mst1/2 D/D) mice were generated to conditionally delete Mst1 and Mst2 from non-ciliated, secretory bronchiolar epithelial cells. Adult mice were maintained on doxycycline food for 16 days to induce deletion of Mst1/2. Lin-/CD326+/CD24-intermediate cells were isolated by fluorescence cell sorting to enrich for the targeted airway epithelial cells. mRNA isolated from Lin-/CD326+/CD24-intermediate cells from control and Mst1/2 D/D mice was pooled and analyzed by RNA-seq to identify transcriptional changes following deletion of Mst1 and Mst2 from mature lung bronchiolar epithelial cells.

2015-01-01 | E-GEOD-61627 | biostudies-arrayexpress

Gene expression profile of mouse liver cancer (Sav1 and Mst1/2 Knockout models)

Project description:Hippo pathway is evolutionarily well conserved. All core components of the pathway identified to date have one or more mammalian orthologs, including MST1/2 (Hippo), SAV1 (Salvador, also known as WW45), LATS1/2 (Warts), MOB1 (Mats), YAP1 and its paralog WWTR1 (also known as TAZ) (Yorkie), and TEAD1/2/3/4 (Scalloped). Ectopic over-expression of YAP1 in mouse liver led to develop hepatocellular carcinoma (HCC). HCC is the third most common cause of cancer-related death in the world, and accounts for an estimated 600,000 deaths annually. Lack of molecular classification and clinical heterogeneity of this malignant disease hampered the development of standardized treatment. To investigate roles of Hippo pathway in liver carcinogenesis, we generated liver-specific Mst1/2 -/- and Sav1 -/- mouse models and collected gene expression data from them. Our study provided new understanding on molecular characteristics of HCC. Sav1 and Mst1/2 Knockout models

2014-08-23 | E-GEOD-32510 | biostudies-arrayexpress

Characterization of Affinity Purifications of full length MST2 and exon 7 deleted MST2 by mass spectrometry

Project description:Hippo is a tumor suppressor pathway and is related to the regulation of cell proliferation, apoptosis, organ size and tumorigenesis. In mammals, the Hippo pathway core is composed of 4 serine-threonine kinases: Mammalian Ste-20-like Kinase 1 and 2 (MST1 and MST2) and large suppressive tumor 1 and 2 (LATS1 and LATS2). When Hippo is active, the transcription co-activators YAP and TAZ are phosphorylated and retained in the cytoplasm. However, when the pathway is inactive, YAP and TAZ are not phosphorylated and enter the cell nucleus, where they activate transcription factors, increasing proliferation and inducing malignant phenotype in epithelial cells. Preliminary results from our laboratory showed that in malignant cells (T4-2), STK3 mRNA (gene encoding MST2) is shorter, a result of an exon skipping splicing that excludes exon 7 from the transcript (STK3delexon7). Analysis of RNAseq data from The Cancer Genome Atlas (TCGA) revealed that the variant STK3delexon7 is also found in samples from patients with breast cancer. We observed that with the exclusion of exon 7 the transcript is translated into a protein that is more susceptible to degradation. Therefore, we wanted to characterize the protein complex of the exon 7 excluded transcript and the full-length protein. To this end, we transfected HEK293-T cells with flag tagged version of full length MST2 and MST2 with the deletion of exon-7. We performed affinity purification of these proteins and characterized their binding partners using mass spectrometry.

2022-04-29 | MSV000089341 | MassIVE

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