Expression Data from Ectopic expression of SUMO-1 in C. elegans
Ontology highlight
ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE19972 | GEO | 2011/01/31
SECONDARY ACCESSION(S): PRJNA122625
REPOSITORIES: GEO
Similar Datasets
Project description:Transgenic C. elegans strains that express human SUMO-1 under the control of pan-neuronal (aex-3) or pan muscular (myo-4) promoters were assayed for gene expression changes. Control N2 non transgenic worms were compared to aex-3::His-SUMO-1 and myo-4::His-SUMO-1 worms in 3 biological replicate populations
2011-01-31 | E-GEOD-19972 | biostudies-arrayexpress
Project description:Comprehensive list of SUMO targets from the nematode Caenorhabditis elegans. SUMO conjugates isolated from transgenic worms carrying 8His and GFP tagged SUMO. The constructs rescues the lethal knock-out of a single SUMO gene, smo-1. SUMO conjugates where isolated from heat shock, arsenite exposure, and UV treated SUMO-GFP worms as well as from control non treated animals. In parallel identical purification procedure was performed with non-transgenic worms and proteins identified with this control where excluded.
2018-01-24 | PXD006644 | Pride
Project description:Expansion of a polyglutamine (polyQ) tract in the gene for the androgen receptor (AR) results in partial loss of transactivation function and causes spinobulbar muscular atrophy (SBMA). Modification of AR by small ubiquitin-like modifier (SUMO) reduces AR function in a promoter context-dependent manner. We used microarrays to confirm and demonstrate loss of AR function from polyQ expansion and to test the degree to which AR function is altered by preventing polyQ AR SUMOylation.
2014-08-23 | GSE50383 | GEO
Project description:Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Keywords: embryonic muscle, myo-3::GFP
2007-07-13 | GSE8462 | GEO
Project description:Expansion of a polyglutamine (polyQ) tract in the gene for the androgen receptor (AR) results in partial loss of transactivation function and causes spinobulbar muscular atrophy (SBMA). Modification of AR by small ubiquitin-like modifier (SUMO) reduces AR function in a promoter context-dependent manner. We used microarrays to confirm and demonstrate loss of AR function from polyQ expansion and to test the degree to which AR function is altered by preventing polyQ AR SUMOylation. PC12 cells expressing AR10Q, AR112Q, or nonSUMOylatable AR112Q (KRKR) in the presence or absence of synthetic androgen R1881 were assessed for alterations in AR function by comparing gene expression changes with each AR variant in response to ligand.
2014-08-23 | E-GEOD-50383 | biostudies-arrayexpress
Project description:Mouse embryonic fibroblasts (MEFs) were generated from Ubc9fl/- and Ubc9+/+ embryos (E13.5). MEFs were treated with tamoxifen for six days to cause CreERT2 activation, and induce Ubc9 floxed allele deletion. We determined the ChIP-seq profiles of SUMO-1 and SUMO-2 using chromatin of wild-type MEFs Ubc9+/+ and of the corresponding Ubc9 KO MEFs which are entirely depleted for sumoylation. The analysis revealed the nearly complete absence of genome-wide binding of SUMO-1 and SUMO-2 in Ubc9-/- MEFs, attesting for antibody specificities.
2018-10-24 | GSE115842 | GEO
Project description:Background: The force generating mechanism of muscle is evolutionarily ancient; the fundamental structural and functional components of the sarcomere are common to motile animals throughout phylogeny. Recent evidence suggests that the transcription factors that regulate muscle development are also conserved. Thus, a comprehensive description of muscle gene expression in a simple model organism should define a basic muscle transcriptome that is also expressed in animals with more complex body plans. To this end, we have applied Micro-Array Profiling of Caenorhabditis elegans Cells (MAPCeL) to muscle cell populations extracted from developing Caenorhabditis elegans embryos. Results: Fluorescence Activated Cell Sorting (FACS) was used to isolate myo-3::GFP-positive muscle cells, and their cultured derivatives, from dissociated early Caenorhabditis elegans embryos. Microarray analysis identified 6,693 expressed genes, 1,305 of which are enriched in the myo-3::GFP positive cell population relative to the average embryonic cell. The muscle-enriched gene set was validated by comparisons to known muscle markers, independently derived expression data, and GFP reporters in transgenic strains. These results confirm the utility of MAPCeL for cell type-specific expression profiling and reveal that 60% of these transcripts have human homologs. Conclusions: This study provides a comprehensive description of gene expression in developing Caenorhabditis elegans embryonic muscle cells. The finding that over half of these muscle-enriched transcripts encode proteins with human homologs suggests that mutant analysis of these genes in Caenorhabditis elegans could reveal evolutionarily conserved models of muscle gene function with ready application to human muscle pathologies. Experiment Overall Design: Our goal is to profile gene expression in the major excitable tissues of Caenorhabditis elegans. As part of this effort, we profiled embryonic muscle cells at two timepoints: 0hr and 24hr.. To isolate transcripts from these cells we utilized the MAPCeL (Microarray Profiling Caenorhabditis elegans Cells) technique, which our lab previously developed (Fox et al 2005) in which myo-3::GFP+ cells are captured by FACS for RNA isolation. We verified these data by bioinformatic means and by in vivo validation by creating GFP reporters for a random set of genes in our enriched gene list.
2008-06-16 | E-GEOD-8462 | biostudies-arrayexpress
Project description:Transient brain ischemia massively activates global SUMOylation. A large fraction of SUMO targets are nuclear proteins involved in gene expression. However, gene expression profile modulated by ischemia-induced SUMOylation has not been studied. Using a SUMO knockdown (SUMO-KD) mouse model and microarray technique, we investigated how SUMOylation modulated gene expression after brain ischemia. Wild-type and SUMO-KD mice were subjected to transient forebrain ischemia or sham surgery. The hippocampal CA1 subfield samples collected at 3 hours reperfusion were analyzed using Affymetrix microarrays.
2016-08-01 | E-GEOD-80681 | biostudies-arrayexpress
Project description:Transient brain ischemia massively activates global SUMOylation. A large fraction of SUMO targets are nuclear proteins involved in gene expression. However, gene expression profile modulated by ischemia-induced SUMOylation has not been studied. Using a SUMO knockdown (SUMO-KD) mouse model and microarray technique, we investigated how SUMOylation modulated gene expression after brain ischemia.
2016-08-01 | GSE80681 | GEO
Project description:Similar to ubiquitin, SUMO forms chains, but the identity of SUMO-chain-modified factors and the purpose of this modification remain largely unknown. Here, we identify budding yeast SUMO protease Ulp2, able to disassemble SUMO chains, as a DDK interactor enriched at replication origins that promotes DNA replication initiation. Replication-engaged DDK is SUMOylated on chromatin, becoming a degradation-prone substrate when Ulp2 no longer protects it against SUMO-chain assembly. Specifically, SUMO chains channel DDK for SUMO-targeted ubiquitin ligase Slx5/Slx8-mediated and Cdc48 segregase-assisted proteasomal degradation. Importantly, the SUMOylation-defective ddk-KR mutant rescues inefficient replication onset and MCM activation in cells lacking Ulp2, suggesting that SUMO chains time DDK degradation. Using two unbiased proteomic approaches, we further identify subunits of the MCM helicase and other factors as SUMO-chain-modified degradation-prone substrates of Ulp2 and Slx5/Slx8. We thus propose SUMO-chain-/Ulp2-protease-regulated proteasomal degradation as a mechanism that times the availability of functionally-engaged SUMO-modified protein pools during replication and beyond.
2019-09-10 | GSE113835 | GEO