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Differentially regulated genes in adipocytes derived from Men1-null vs WT mouse embryonic stem cells

ABSTRACT: MEN1 is a tumor suppressor gene loss of which causes lipoma (fatty tumors under the skin) and many other endocrine and non-endocrine tumors. It's target genes in fat cells (adipocytes) are unknown. Gene expression in adipocytes that were in vitro differentiated from mouse embryonic stem cells (mESCs) of Men1-nul l(Men1-KO) and WT mice were compared to assess the expression of genes upon menin loss in adipocytes that could lead to the deveopment of lipoma. mESCs (Men1-null and WT) were in vitro differentaited into adipocytes. Positive oil red O staining indicated successful differentiation into adipocytes. The cells were processed for RNA isolation. RNA preps were used for microarray analysis.

ORGANISM(S): Mus musculus

SUBMITTER: WeiPing Chen

PROVIDER: E-GEOD-65859 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Consequence of Menin Deficiency in Mouse Adipocytes Derived by In Vitro Differentiation.

Parekh Vaishali I VI Modali Sita D SD Desai Shruti S SS Agarwal Sunita K SK

International journal of endocrinology 20150702

Lipoma in patients with the multiple endocrine neoplasia type 1 (MEN1) syndrome is a type of benign fat-cell tumor that has biallelic inactivation of MEN1 that encodes menin and could serve as a model to investigate normal and pathologic fat-cell (adipocyte) proliferation and function. The role of menin and its target genes in adipocytes is not known. We used in vitro differentiation to derive matched normal and menin-deficient adipocytes from wild type (WT) and menin-null (Men1-KO) mouse embryo ...[more]

PMID: 26229531

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Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (ChIP-Seq)

Project description:Inactivating mutations in the MEN1 gene predisposing to the multiple endocrine neoplasia type 1 (MEN1) syndrome can also cause sporadic pancreatic endocrine tumors. MEN1 encodes menin, a subunit of MLL1/MLL2-containing histone methyltransferase complexes that trimethylate histone H3 at lysine 4 (H3K4me3). The importance of menin-dependent H3K4me3 in normal and transformed pancreatic endocrine cells is unclear. To study the role of menin-dependent H3K4me3, we performed in vitro differentiation of wild-type as well as menin-null mouse embryonic stem cells (mESCs) into pancreatic islet-like endocrine cells (PILECs). Gene expression analysis and genome-wide H3K4me3 ChIP-Seq profiling in wild-type and menin-null mESCs and PILECs revealed menin-dependent H3K4me3 at the imprinted Dlk1-Meg3 locus in mESCs, and all four Hox loci in differentiated PILECs. Specific and significant loss of H3K4me3 and gene expression was observed for genes within the imprinted Dlk1-Meg3 locus in menin-null mESCs and the Hox loci in menin-null PILECs. Given that the reduced expression of genes within the DLK1-MEG3 locus and the HOX loci is associated with MEN1-like sporadic tumors, our data suggests a possible role for menin-dependent H3K4me3 at these genes in the initiation and progression of sporadic pancreatic endocrine tumors. Furthermore, our investigation also demonstrates that menin-null mESCs can be differentiated in vitro into islet-like endocrine cells, underscoring the utility of menin-null mESC-derived specialized cell types for genome-wide high-throughput studies. Genome-wide mapping of H3K4me3 and microarray gene expression profiling in TC-1 wild-type (WT) mESCs, menin-null (Men1-ko) mESCs (3.2N), pancreatic islet-like endocrine cells (PILECs) derived from WT mESCs, and PILECs derived from Men1-ko mESCs.

2012-06-01 | E-GEOD-37774 | biostudies-arrayexpress

Differentially regulated genes in adipocytes derived from Men1-null vs WT mouse embryonic stem cells

Project description:MEN1 is a tumor suppressor gene loss of which causes lipoma (fatty tumors under the skin) and many other endocrine and non-endocrine tumors. It's target genes in fat cells (adipocytes) are unknown. Gene expression in adipocytes that were in vitro differentiated from mouse embryonic stem cells (mESCs) of Men1-nul l(Men1-KO) and WT mice were compared to assess the expression of genes upon menin loss in adipocytes that could lead to the deveopment of lipoma.

2016-02-03 | GSE65859 | GEO

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors

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DOT1 Like Histone Lysine Methyltransferase (DOT1L) and Menin 1 (MEN1) interaction proteomics in breast cancer cell nuclei

Project description:Estrogen Receptor alpha (ERα) is a ligand-inducible transcription factor that mediates estrogen signaling in hormone-responsive breast cancer (BC) and is the primary target of specific anticancer therapies that although effective can generate resistance phenomena that represents a crucial problem in clinical management of patients affected by this disease. DOT1 Like Histone Lysine Methyltransferase (DOT1L) and Menin 1 (MEN1) have been identified as functional component of the ERα mechanism of action. To investigate the involvement of DOT1L and MEN1 in mediating ERα actions in hormone-responsive and endocrine-resistant BC, interaction proteomics was applied to map the DOT1l and MEN1 nuclear interacting partners in MCF7 breast cancer cell nuclei in order to the identifiy new possible therapeutic targets for a more effective pharmacological treatment of endocrine therapy-resistant tumors.

2022-08-12 | PXD026864 | Pride

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (mRNA)

2012-05-31 | E-GEOD-37775 | biostudies-arrayexpress

A cDNA microarray analysis was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1

Project description:Menin, the product of the MEN1 gene in humans (Men1 in mice), is responsible for the inherited tumor syndrome, multiple endocrine neoplasia type 1 (MEN1). menin interacts with the trithorax group (trxG) proteins (Drosophila) and the mixed-lineage leukemia (MLL) (humans) histone methyltransferase (HMTase) complex, and it alters histone tail modifications and the transcription of target genes. To explore a potential functional implication of menin in HCC, we stably transfected HepG2 or L-02 cells with either vectors or constructs expressing MEN1. A cDNA microarray analysis was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1. To obtain a broader understanding of the molecular network of menin in HCC, the whole genome microarray expression profiling was performed on HepG2 or L-02 cells with either vectors or constructs expressing MEN1. Comparison of gene expression results from HepG2 or L-02 cells with either vectors or constructs expressing MEN1.

2015-07-07 | E-GEOD-70556 | biostudies-arrayexpress

Genome-wide identification of Ago2 binding sites from mouse embryonic stem cells with and without mature microRNAs

Project description:MicroRNAs (miRNAs) are a large family of 19-22nt non-coding RNAs that post-transcriptionally regulate their mRNA targets. Computational algorithms predict that over half of all genes are regulated by miRNAs, yet approaches for experimental identification of miRNA binding sites are now emerging. To directly identify endogenous miRNA binding sites, we performed photo-crosslinking immunoprecipitation using antibodies against Ago2, followed by deep-sequencing of RNA tags (CLIP-seq) in mouse embryonic stem cells (mESCs). We also performed parallel CLIP-seq in Dicer null mESCs that lack mature miRNAs, allowing us to define whether the association of Ago2 with the identified sites was mediated by miRNAs. We include the exon-array expression data obtained from three sets of Dicer WT and Dicer Null mESCs.These data are used to determine genes that are differentially expressed between Dicer WT and Dicer Null conditions. Six samples (3 Dicer wild-type CLIP RNA libraries representing two biological replicates, 2 Dicer null CLIP RNA libraries, 1 short-RNA library from Dicer wild-type mESCs) were analyzed. Six total mESC samples were analyzed (3 Dicer WT, 3 Dicer Null). Expression values for probesets were summarized into a single per-gene value. The log fold change for Dicer_WT/Dicer_Null was defined as the difference between the mean expression in Dicer WT mESCs and the mean expression in the Dicer Null mESCs.

2011-01-10 | E-GEOD-25310 | biostudies-arrayexpress

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (mRNA)

2012-06-01 | GSE37775 | GEO

Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (ChIP-Seq)

2012-06-01 | GSE37774 | GEO

Transcriptional profiling by array of Klf2 wild-type and Klf2-Null mESCs cultured under 2i

Project description:The self-renewing pluripotent state was first captured in mouse embryonic stem cells (mESCs) over two decades ago. The standard condition requires the presence of serum and LIF, which provide growth promoting signals for cell expansion. However, there are pro-differentiation signals which destabilize the undifferentiated state of mESCs. The dual inhibition (2i) of the pro-differentiation Mek/Erk and Gsk3/Tcf3 pathways in mESCs is sufficient to establish an enhanced pluripotent “ground state” which bears features resembling the pre-implantation mouse epiblast. Gsk3 inhibition alleviates the repression of Esrrb, a transcription factor that can substitute for Nanog function in mESCs. The molecular mechanism that is mediated by Mek inhibition is however not clear. In this study, we investigate the pathway through which Mek inhibition operates to maintain ground state pluripotency. We have found that in mESCs, Kruppel-like factor 2 (Klf2) is a protein target of the Mek/Erk pathway; and that Klf2 protein is phosphorylated by Erk2 and subsequently degraded through the proteosome. It is therefore by Mek-inhibition through PD0325901 or 2i that enables the stabilization and accumulation of Klf2 to sustain ground state pluripotency. Importantly, we found that Klf2-null mESCs, while viable under LIF/Serum conditions, cannot be maintained and eventually gradually die within a few passages. Our result thus demonstrates that Klf2 is an essential factor of ground state pluripotency. Collectively, our study defines the Mek/Klf2 axis that cooperates with the Gsk3/Esrrb pathway in mediating ground state pluripotency.

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