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Expression values from wild-type retinas and retinas with a mutant Rhodopsin transgene (Tg(RHO P347S)) with and without Endothelin-2 (EDN2)

ABSTRACT: Expression of the Endothelin-2 (Edn2) mRNA is greatly increased in the photoreceptors (PRs) of mouse models of inherited PR degeneration. To identify retinasl gene whose expression is directly or indirectly regulated by EDN2 in the presence of the Tg(RHO P347S) mutant allele, we defined mRNAs that were differentially expressed in Edn2+/+, Edn2-/-, Tg(RHO P347S) Edn2+/+, and Tg(RHO P347S) Edn2-/- retinas.

ORGANISM(S): Mus musculus

PROVIDER: GSE38797 | GEO | 2012/07/16

SECONDARY ACCESSION(S): PRJNA168640

REPOSITORIES: GEO

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Expression values from wild-type retinas and retinas with a mutant Rhodopsin transgene (Tg(RHO P347S)) with and without Endothelin-2 (EDN2)

Project description:Expression of the Endothelin-2 (Edn2) mRNA is greatly increased in the photoreceptors (PRs) of mouse models of inherited PR degeneration. To identify retinasl gene whose expression is directly or indirectly regulated by EDN2 in the presence of the Tg(RHO P347S) mutant allele, we defined mRNAs that were differentially expressed in Edn2+/+, Edn2-/-, Tg(RHO P347S) Edn2+/+, and Tg(RHO P347S) Edn2-/- retinas. RNA was extracted from Edn2+/+, Edn2-/-, Tg(RHO P347S) Edn2+/+, and Tg(RHO P347S) Edn2-/- retinas at postnatal day 21 (PN21) and hybridized to Affymetrix arrays

2012-07-15 | E-GEOD-38797 | biostudies-arrayexpress

Endothelin2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis

Project description:Endothelin signaling is required for neural crest migration and homeostatic regulation of blood pressure. Here we report that constitutive over-expression of Endothelin-2 (Edn2) in the mouse retina perturbs vascular development by inhibiting endothelial cell (EC) migration across the retinal surface and subsequent EC invasion into the retina. Developing endothelial cells exist in one of two states: tip cells at the growing front, and stalk cells in the vascular plexus behind the front. This division of endothelial cell states is one of the central organizing principle of angiogenesis. In the developing retina, Edn2 over-expression leads to over-production of endothelial tip cells by both morphologic and molecular criteria. Spatially localized over-expression of Edn2 produces a correspondingly localized endothelial response. Edn2 over-expression in the early embryo inhibits vascular development at mid-gestation, but Edn2 over-expression in developing skin and brain has no discernable effect on vascular structure. Inhibition of retinal angiogenesis by Edn2 requires expression of Endothelin receptor A (Ednra) but not Ednrb in the neural retina. Taken together, these observations imply that the neural retina responds to Edn2 by synthesizing one or more factors that promote the endothelial tip cell state and inhibit angiogenesis. The response to Edn2 is sufficiently potent that it over-rides the activities of other homeostatic regulators of angiogenesis, such as vascular endothelial growth factor.

2014-01-01 | GSE50059 | GEO

Endothelin2 signaling in the neural retina promotes the endothelial tip cell state and inhibits angiogenesis

2014-01-01 | E-GEOD-50059 | biostudies-arrayexpress

Mus musculus

Project description:Expression values from wild-type retinas and retinas with a mutant Rhodopsin transgene (Tg(RHO P347S)) with and without Endothelin-2 (EDN2)

| PRJNA168640 | ENA

Phosphoproteomics of endothelin signalling

Project description:Time resolved phosphorylation changes were measured the melanoma cell lines A2058 and UACC257. An endothelin B receptor knockout of UACC257 was processed in parallel. Protein abundance was also compared at the latest time point of the study (90 min) using DIA-SWATH

2019-10-09 | PXD012316 | Pride

Endothelin signaling activates neural crest gene expression via a MEF2C-dependent positive-feedback transcriptional mechanism

Project description:Endothelin signaling is one of the essential signaling pathways that control vertebrate development. Dysregulated Endothelin signaling plays an important role in the pathogenesis of human diseases such as Hirschsprung’s disease, pulmonary hypertension and cancer. However, the downstream transcriptional program and transcriptional factors of Endothelin signaling have been incompletely understood. Here, we used RNA-sequencing to identify the genes regulated by Endothelin signaling in the neural crest, where Endothelin signaling functions primarily during development. We further demonstrate that Endothelin induces gene expression through the de-repression of the MADS Box transcription factor MEF2C. Moreover, in the Mef2c gene locus, we identified an Endothelin responsive cis-regulatory element which functions as a central component of an Endothelin-MEF2C positive feedback transcriptional mechanism that regulates downstream gene expression.

2016-11-15 | GSE47919 | GEO

E. coli MG1655Δrac treated (N340S/G324D Rho) vs control (WT Rho)

Project description:Transcription profiling of E. coli MG1655Δrac, comparing the effect Rho mutants (SBS: N340S, G324D) with WT Rho

2016-03-28 | GSE77177 | GEO

Transcription profiling of E. coli inhibited for Rho activity to assess Rho function

Project description:Transcription termination factor Rho is essential in enterobacteria. We inhibited Rho activity with bicyclomycin and used microarray experiments to assess Rho function on a genome-wide scale. Rho is a global regulator of gene expression that matches E. coli transcription to translational needs. Remarkably, genes that are most repressed by Rho are prophages and other horizontally-acquired portions of the genome. Elimination of these foreign DNA elements increases resistance to bicyclomycin. Although rho remains essential, such reduced-genome bacteria no longer require Rho cofactors NusA and NusG. Thus, Rho termination, supported by NusA and NusG, is required to suppress the toxic activity of foreign DNA. Global regulation of transcription termination by Rho, NusA, and NusG. Experiment Overall Design: Two sets of experiments are presented. First, treatment of E. coli with Rho inhibitor bicyclomycin was performed in strains MG1655 and O157:H7 EDL933 for twenty minutes at concentrations of 10, 25, or 100 micrograms/milliliter. In the second set of experiments the reduced-genome strain MDS42 was treated with bicyclomycin as well as having deletions of the genes nusA and nusG. Total RNA was extracted and hybridized to the Affymetrix E. coli Genome 2.0 array, which contains complete genome coverage of four strains of E. coli.

2008-06-20 | E-GEOD-10345 | biostudies-arrayexpress

E. coli MG1655Î?rac treated (N340S/G324D Rho) vs control (WT Rho)

Project description:Transcription profiling of E. coli MG1655Î?rac, comparing the effect Rho mutants (SBS: N340S, G324D) with WT Rho Organism: Escherichia coli ,Agilent Custom Escherichia coli Gene Expression Microarray 8x15K (AMADID: 020304) designed by Genotypic Technology Private Limited.

2016-03-28 | E-GEOD-77177 | biostudies-arrayexpress

Rho stimulates both Rho-dependent and intrinsic termination in Bacillus subtilis

Project description:In this work we conducted Term-seq on Wild Type B. subtilis, and strains compromosing all logical mutations in all combinations of the genes that encode for NusA, NusG, and Rho, where we developed the first transcription termination atlas. We used this atlas to find that Rho can stimulate intrinsic termination in B. subtilis and we recapitulated this finding in vitro to dissect the mechanism.

2022-08-11 | GSE188366 | GEO

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