Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Menin links the stress response to genome stability in Drosophila melanogaster

ABSTRACT: Mutants of the Mnn1 gene are hyper-sensitive to several stresses and display increased genome instability when subjected to conditions, such as heat shock, generally regarded as non-genotoxic. We describe a role for Menin as a global regulator of heat shock gene expression and critical factor in the maintenance of genome integrity

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE20497 | GEO | 2010/10/25

SECONDARY ACCESSION(S): PRJNA125075

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Menin links the stress response to genome stability in Drosophila melanogaster

Project description:Mutants of the Mnn1 gene are hyper-sensitive to several stresses and display increased genome instability when subjected to conditions, such as heat shock, generally regarded as non-genotoxic. We describe a role for Menin as a global regulator of heat shock gene expression and critical factor in the maintenance of genome integrity 2-colour microarray design using 36 microarrays testing shock vs non shock in Drosophila melanogaster. Using a test of loss-of-heterozygosity, we show that Drosophila strains lacking a functional Mnn1 gene or expressing a Mnn1 dsRNAi are characterized by increased genome instability in response to short, repeated but non-lethal heat shock or hypoxia treatments. The same was true for strains lacking all Hsp70 genes.

2010-10-25 | E-GEOD-20497 | biostudies-arrayexpress

Menin links the stress response to genome stability in Drosophila melanogaster.

Project description: Not available

| S-EPMC2987805 | biostudies-literature

Investigation of Alterations in Gene Expression in the Retina Induced by Intravitreal Injection of SH-42 and SH-80

Project description:In this study, we demonstrate that SH-42 and SH-80, novel heat shock protein 90 inhibitors, suppress retinal neovascularization via inhibition of hypoxia-mediated angiogenesis. To figure out any genotoxic effect of these compounds related with heat shock protein 90 inhibition, we performed microarray analyses with retinal tissues treated with SH-42 and SH-80 for 7 days. We intravitreally injected PBS, SH42, or SH80 into the right eyes of C57BL/6 male mice (n = 12 per group). PBS-treated mice were regarded as negative control. Four retinal tissues were pooled into 1 test tube and prepared for further analyses.

2013-04-16 | E-GEOD-46057 | biostudies-arrayexpress

NHGRI Menin ChIP-Chip

Project description:Multiple endocrine neoplasia type I (MEN1) is a familial cancer syndrome characterized primarily by tumors of multiple endocrine glands. The gene for MEN1 encodes a ubiquitously expressed tumor suppressor protein called menin. Menin was recently shown to interact with several components of a trithorax family histone methyltransferase complex including ASH2, Rbbp5, WDR5, and the leukemia proto-oncoprotein MLL. To elucidate menin's role as a tumor suppressor and gain insights into the endocrine-specific tumor phenotype in MEN1, we mapped the genomic binding sites of menin, MLL1, and Rbbp5, to approximately 20,000 promoters in HeLa S3, HepG2, and pancreatic islet cells using the strategy of chromatin-immunoprecipitation coupled with microarray analysis. We found that menin, MLL1, and Rbbp5 localize to the promoters of thousands of human genes but do not always bind together. These data suggest that menin functions as a general regulator of transcription. Keywords: ChIP/chip NHGRI Menin ChIP-Chip

2006-07-24 | E-GEOD-5357 | 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

Project description:This SuperSeries is composed of the following subset Series: GSE37774: 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) GSE37775: Genome-wide characterization of menin-dependent H3K4me3 reveals a specific role for menin in the regulation of genes implicated in MEN1-like tumors (mRNA) Refer to individual Series

2012-05-31 | E-GEOD-37776 | 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)

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.

2012-05-31 | E-GEOD-37775 | 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 (ChIP-Seq)

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

Menin-regulated genes in bone marrow B-cell progenitors

Project description:MLL1 translocations encode fusion proteins retaining the N-terminus of MLL1, which interacts with the tumor suppressor, menin. This interaction is essential for leukemogenesis, thus is a promising drug target. However, wild-type MLL1 plays a critical role in sustaining hematopoietic stem cells (HSCs), therefore disruption of an essential MLL1 cofactor would be expected to obliterate normal hematopoiesis. Here we show that rather than working together as a complex, menin and MLL1 regulate distinct pathways during normal hematopoiesis, particularly in HSCs and B-cells. We demonstrate the lack of genetic interaction between menin and MLL1 in steady-state or regenerative hematopoiesis and in B-cell differentiation despite the fact that MLL1 is critical for these processes. In B-cells, menin- or MLL1-regulated genes can be classified into three categories: 1) a relatively small group of co-regulated genes including previously described targets Hoxa9 and Meis1 but also Mecom and Eya1, and much larger groups of 2) exclusively menin-regulated and 3) exclusively MLL1-regulated genes. Our results highlight the large degree of independence of these two proteins and demonstrate that menin is not a requisite cofactor for MLL1 during normal hematopoiesis. Furthermore, our data support the development of menin-MLL1 disrupting drugs as safe and selective leukemia targeting agents. We performed gene expression analysis to determine the genes deregulated in B-cell progenitors upon loss of menin. Fraction B pro-B cells (defined as B220+CD43+HSA+BP-1- BM cells) were sorted from four MenF/F and four Rag1-cre;MenF/F mice of three weeks old. Total RNA was amplified once, labeled, fragmented and hybridized to Affymerix GeneChip Mouse Genome 430 2.0 array.

2013-08-05 | E-GEOD-49120 | biostudies-arrayexpress

Investigation of Alterations in Gene Expression in the Retina Induced by Intravitreal Injection of SH-42 and SH-80

2013-04-16 | GSE46057 | GEO

Whole-genome analysis of heat shock factor binding sites in Drosophila melanogaster at room temperature

Project description:Whole-genome analysis of heat shock factor binding sites in Drosophila melanogaster. Heat shock factor IP DNA from non-shock (room temperature) Kc 167 cells compared to whole cell extract on Agilent 2x244k tiling arrays.

2011-01-05 | GSE22335 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data