Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profiling of C. elegans sma-9 and dbl-1 gene knock-outs

ABSTRACT: Experiments performed to determine target genes of sma-9 and DBL-1 signaling

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Ling Yu

PROVIDER: E-MEXP-687 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Transcriptional repressor and activator activities of SMA-9 contribute differentially to BMP-related signaling outputs.

Liang Jun J Yu Ling L Yin Jianghua J Savage-Dunn Cathy C

Developmental biology 20070303 2

In the nematode Caenorhabditis elegans, the BMP-related growth factor DBL-1 regulates body size and male tail morphogenesis via a conserved receptor/Smad signaling pathway. Smads are transcription factors, but rely on transcription cofactors for appropriate regulation of target genes in response to TGF-beta- and BMP-related signals. In the DBL-1 pathway, sma-9 encodes multiple zinc finger transcription factors homologous to Drosophila Schnurri, which functions in Dpp/BMP signaling. We have studi ...[more]

PMID: 17397820

Similar Datasets

CHN-1 and CHN-1 L141R interacting proteins

Project description:Proteostasis is achieved by quality control pathways that support the generation of correctly folded proteins, prevent protein misfolding and remove toxic proteins. The quality control E3 ligase CHIP ubiquitylates damaged proteins consigned by chaperone partners for disposal through the endo-lysosomal pathway, proteasomal degradation, or autophagy. Additionally, CHIP has been reported to modulate essential signaling pathways by precisely delivering a myriad of native proteins to destined fates. We aimed at understanding the substrate specificity and processivity through a “structure to function” approach, by examining the modeled 3D structure of the C. elegans ortholog of CHIP, CHN-1, based on the reported structure of murine CHIP. Using different model organisms and various genetic and biochemical analyses, we demonstrate that monomeric CHN-1/CHIP has preserved ubiquitylation activity and promotes longevity via the IIS pathway. The lack of monomer results in premature aging and neurodegenerative disorder. Our data reveal that autoubiquitylation plays an important role in the alteration between monomer and dimer. Together, the conserved dimer-monomer transition provides a molecular switch regulating CHIP activity in response to proteotoxic stress and aging.

2022-08-25 | PXD025375 | Pride

Caenorhabditis elegans mRBPome

Project description:This project aims to identify novel RNA binding proteins in the nematode, Caenorhabditis elegans. Since interactions between RNAs and proteins may be transient, these animals were crosslinked with UV light at 254 nm which promotes the covalent link between proteins and RNAs. After this, polyadenylated mRNAs were purified via oligo(dT) coupled to magentic beads under stringent conditions. Finally, samples were subjected to mass spectrometry analysis. To rule out the possibility of RNA-independent binding we also analysed other samples: i) samples digested with RNase one; ii) samples where we performed competition assays with polyadenylic acid

2015-10-26 | PXD002226 | Pride

H3K4me2 regulates the recovery of protein biosynthesis and homeostasis from UV-induced DNA damage during development and aging

Project description:DNA damage causes cancer, impairs development and accelerates aging. UV irradiation induces transcription-blocking lesions and defects in transcription-coupled nucleotide excision repair lead to developmental failure and premature aging in humans. Following DNA repair, the homeostatic processes need to be reestablished to ensure development and maintain tissue functionality. Here, we report that in C. elegans removal of the MLL/COMPASS H3K4 methyltransferase exacerbates the developmental growth retardation and accelerates aging, while depletion of the H3K4 demethylase, SPR-5, promotes developmental growth and extends lifespan amid UV-induced damage. We demonstrate that specifically the DDR-induced H3K4me2 is associated with the activation of genes regulating RNA transport, splicing, ribosome biogenesis, and protein homeostasis and regulates the recovery of protein biosynthesis that is essential for survival of UV-induced DNA damage. Our study uncovers a role of H3K4me2 in coordinating the recovery of protein biosynthesis and homeostasis that is required for developmental growth and longevity after DNA damage.

2020-10-13 | PXD015354 | Pride

Mechanisms of stop codon readthrough mitigation reveal principles of GCN1 mediated translational quality control

Project description:Readthrough into the 3′ untranslated region (3′UTR) of the mRNA results in the production of aberrant proteins. Metazoans efficiently clear readthrough proteins, but the underlying mechanisms remain unknown. Here, we show in C. elegans and mammalian cells that readthrough proteins are targeted by a coupled, two-level quality control pathway involving the BAG6 chaperone complex and the ribosome collision-sensing protein GCN1. Readthrough proteins with hydrophobic C-terminal extensions are recognized by SGTA-BAG6 and ubiquitylated by RNF126 for proteasomal degradation. Additionally, cotranslational mRNA decay initiated by GCN1 and CCR4/NOT limits the accumulation of readthrough products. Unexpectedly, selective ribosome profiling uncovered a general role of GCN1 in regulating translation dynamics when ribosomes encounter nonoptimal codons, a feature of 3′UTR sequences. Dysfunction of GCN1 results in mRNA and proteome imbalance, increasingly perturbing transmembrane proteins and collagens during aging. These results define GCN1 as a key factor acting during translation in maintaining protein homeostasis.

2023-06-09 | PXD037037 | Pride

Phosphoproteomics of C.elegans RNA binding protein mutants

Project description:Nonsense-mediated mRNA decay (NMD) monitors the quality of transcriptomes and degrades messenger RNAs containing splicing errors or premature stop codons. NMD thus dictates the severity and outcome of genetic disorders, gene edits and knockouts as well as the prevalence of neoantigens. Central to the NMD pathway are SMG-1, an ATM/ATR-like kinase, and its downstream target SMG-2/UPF1, a highly processive DNA/RNA helicase. Interestingly, many NMD factors acquired additional ‘moonlighting’ functions in the nucleus, including roles in DNA synthesis and DNA damage signalling. While having the same protein controlling RNA and DNA metabolism could be beneficial, it could also lead to signalling conflicts that jeopardize genome stability. Surprisingly little is known about the incidence and impact of such crosstalk in biology, neither in physiological nor in pathological scenarios. Here, via genetics screens and genome-wide analyses, we identified unforeseen crosstalk between RNA surveillance and DNA repair in living animals. Defects in RNA processing, due to viable THO complex or PNN-1 mutations, trigger SMG-1 activity, which causes a major shift in DNA repair and compromises genome stability in somatic tissues. Mechanistically, we find SMG-1 and SMG-2/UPF1, but not NMD per se, to suppress DNA repair by classical non-homologous end-joining while allowing mutagenic repair by single strand annealing. We postulate that aberrant RNA structures trigger crosstalk that re-directs DNA repair and genome evolution.

2022-08-12 | PXD022616 | Pride

Genome-wide identification of the occupancy of RNA polymerase II (POL II) at L4/young adult stage in C. elegans

Project description:We acquied the RNA polymerase II binding profiles in ama-1 transgenic worms. The large subuint of POL II, AMA-1, was C-terminally tagged with GFP, the binding regions were determined using chromatin immunoprecipitation with anti-GFP and anti-polymerase II antibodies followed by illumina high-throughput sequencing (ChIP-seq). For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf RNA polymerase II binding profiles at L4/young adult stage were acquied with anti-native protein antibody (8WG16) and anti-epitope (GFP) antibody

2009-04-11 | E-GEOD-15535 | biostudies-arrayexpress

Identification of transcription factor MAB-5 binding sites

Project description:We identified the DNA binding sites of MAB-5 in C. elegans. MAB-5 was C-terminally tagged with GFP and the expression pattern was examined through fluorescent microscopy. The binding sites were determined using chromatin immunoprecipitation with anti-GFP antibody followed by illumina high-throughput sequencing (ChIP-seq). For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Identification of MAB-5 binding sites at L3 stage

2009-04-11 | E-GEOD-15625 | biostudies-arrayexpress

Identification of transcription factor DAF-16 binding sites in C. elegans

Project description:We identified the DNA binding sites of DAF-16 in transgenic line TJ356 (daf-16::gfp) that carries high-copy number daf-16. The expression pattern was examined through fluorescent microscopy. The binding sites were determined using chromatin immunoprecipitation with anti-GFP antibody and anti-POL II antibody followed by illumina high-throughput sequencing (ChIP-seq). For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf Identification of DAF-16 binding sites at L4/Young adult stage when DAF-16 was highly overexpressed

2009-04-11 | E-GEOD-15567 | biostudies-arrayexpress

RNAi knock down of daf-2, daf-3, daf-16 in C. elegans over 0-48 hours

Project description:Comparison of sterile worms grown on Control Vector, daf-2 RNAi, and daf-2 + daf-16 RNAi. Synchronized fer-15(b26); fem-1(hc17) animals were grown on RNAi bacteria at 25ºC, induced with IPTG on Day 1 of adulthood, and collected from 0-48 hours (10 time points) and 0-196 hours (10 time points); RNAi bacteria was supplemented as necessary for later time points. Worms were floated off lawns with M9 buffer, centrifuged, and washed again in M9. The pelleted worms were dissolved in Trizol (Gibco) and frozen in liquid nitrogen.Time courses were compared with mixed references (collected from 1/2 of each of the time course samples)

2003-07-17 | E-MEXP-8 | biostudies-arrayexpress

RNAi knock down of daf-16 in C. elegans over 0-192 hours

2003-07-17 | E-MEXP-9 | biostudies-arrayexpress