Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq of Arc/Arg3.1-positive versus Arc/Arg3.1-negative skin migratory dendritic cells from healthy mice

ABSTRACT: The key function of migratory dendritic cells (migDCs) is to take up antigens in peripheral tissues and migrate to draining lymph nodes (dLN) to initiate immune responses. Recently, we discovered in mice that in the immune system activity-regulated cytoskeleton associated protein/activity-regulated gene 3.1 (Arc/Arg3.1) is exclusively expressed by migDCs and is a central driver of fast inflammatory migration. However, the frequency of Arc/Arg3.1 expressing cells in different migDC subsets including Langerhans cells (LC), their phylogenetic origin, transcription factor dependency and functional role remains unclear. Here we found that Arc/Arg3.1+ migDCs derived from common DC precursors (CDPs) and radio-resistant LCs. They were present in all migDC subsets and showed a consistent superiority in inflammatory migration but were independent of the transcription factors Irf4 or Batf3. In intradermal Staphylococcus aureus infection, a model that relies on effective inflammatory antigen transport, Arc/Arg3.1 deletion strongly reduced T cell responses. By contrast, Arc/Arg3.1 deficiency did not hamper the immune response to systemic Listeria monocytogenes infection, which does not require antigen transport. Thus, our results show that Arc/Arg3.1 is a molecular marker for defining a population of DCs with superior migratory capacity that spans across all migDC subsets irrespective of ontogeny and phenotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE116161 | GEO | 2021/06/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Arc/Arg3.1 functionally defines migrating 1 dendritic cells and regulates actin dynamics

Project description:We compared the expression profiles of bone marrow-derived dendritic cells (BMDC) derived from Arc/Arg3.1 knockout and wildtype animals. We generated bone marrow-derived dendritic cells (BMDC) from Arc/Arg3.1 knockout and wildtype animals. BMDC were either stimulated with LPS or left untreated and analysed by microarray.

2015-08-12 | E-GEOD-71937 | biostudies-arrayexpress

Arc/Arg3.1 functionally defines migrating 1 dendritic cells and regulates actin dynamics

Project description:We compared the expression profiles of bone marrow-derived dendritic cells (BMDC) derived from Arc/Arg3.1 knockout and wildtype animals.

2015-08-12 | GSE71937 | GEO

RNA-seq of Arc/Arg3.1-positive versus Arc/Arg3.1-negative skin migratory dendritic cells from healthy mice

Project description:RNA-seq of Arc/Arg3.1-positive versus Arc/Arg3.1-negative skin migratory dendritic cells from healthy mice

| PRJNA477512 | ENA

Detection of Arc/Arg3.1 oligomers in rat brain: constitutive and synaptic activity-evoked dimer expression in vivo

Project description:The immediate early gene product activity-regulated cytoskeleton-associate protein (Arc or Arg3.1) is a major regulator long-term synaptic plasticity with critical roles in postnatal cortical development and memory formation. However, the molecular basis of Arc function is not defined. Arc is a hub protein with interaction partners in the postsynaptic neuronal compartment and nucleus. In vitro biochemical and biophysical analysis of purified recombinant Arc show formation of low-order oligomers and larger particles including retrovirus-like capsids. Here, we provide evidence for naturally occurring Arc oligomers in mammalian brain. Using in situ protein crosslinking to trap weak Arc-Arc interactions, we identified in various preparations a prominent Arc immunoreactive band on SDS-PAGE of molecular mass corresponding to a dimer. While heavier Arc species or putative trimers and tetramers were detected, they were of lower abundance. In the dentate gyrus (DG) of adult anesthetized rats, induction of long-term potentiation (LTP) by high-frequency stimulation (HFS) of medial perforant synapses or by brief intrahippocampal infusion of BDNF led to a massive increase in Arc dimer expression. Arc immunoprecipitation of crosslinked DG tissue showed enhanced expression of dimer during four hours of LTP maintenance. Mass spectrometric proteomic analysis of immunoprecipitated, gel-excised bands corroborated detection of Arc dimer. Furthermore, Arc dimer was constitutively expressed in naïve cortical, hippocampal and DG tissue, with lowest levels in the DG. Taken together the results implicate Arc dimers as the predominant low-oligomeric form in mammalian brain, exhibiting regional differences in its constitutive expression and pronounced enhanced expression during DG LTP.

2023-07-20 | PXD039612 | Pride

Prions induce an early Arc response in the hippocampus of prion-infected mice

Project description:Synapse dysfunction and synaptic loss are a central feature of neurodegenerative disorders, including prion disease. The cellular prion protein (PrPC) binds prion, amyloid-β, tau, and α-synuclein oligomers, resulting in the activation of macromolecular complexes and signaling at the post-synapse, yet the initial signaling events are unclear. Here we used a transcriptomic approach focused on the early-stage, prion-infected hippocampus of male wild type mice, and identify immediate early genes, including the synaptic activity response gene, Arc/Arg3.1, as significantly upregulated. In a longitudinal study of the prion-infected hippocampus, Arc/Arg-3.1 protein increased, from early to terminal disease. Notably, metabotropic glutamate receptor levels (mGluR5 dimers) were markedly reduced over time, while phosphorylated AMPA receptors (pGluA1-S845) levels increased. Sporadic Creutzfeldt-Jakob disease (sCJD) post-mortem cortical samples also showed low levels of mGluR5 dimers. Together, these findings suggest that prions trigger a chronic Arc response, an increase in phosphorylated GluA1, and a reduction in mGluR5 receptors beginning in early disease.

2023-01-01 | GSE207251 | GEO

Endogenous brain ARC complexes

Project description:Arc is an activity regulated neuronal protein yet little is known about its protein interactions, assembly into multiprotein complexes, role in human disease and cognition. We applied an integrated proteomic and genetic strategy using targeted tagging of a Tandem Affinity Purification (TAP) tag and Venus fluorescent protein into the endogenous Arc gene in mice, biochemical and proteomic characterization of native complexes in wild type and knockout mice, and human genetic analyses of disease and intelligence. TAP tagging enabled efficient purification of complexes and identification of many novel Arcinteracting proteins, of which PSD95 was the most abundant. PSD95 was essential for Arc assembly into 1.5 MDa complexes and activity-dependent recruitment to excitatory synapses. Integrating human genetic data with proteomic data showed postsynaptic Arc- PSD95 complexes are enriched in schizophrenia, intellectual disability, autism and epilepsy mutations and normal variants in intelligence. Arc-PSD95 postsynaptic complexes are a molecular substrate for the convergence of normal and pathological genetic variants impacting on human cognitive function.

2017-10-19 | PXD007283 | Pride

Rapid transcription of arc/arg3.1 and other very fast immediate early genes in response to neuronal activity is mediated by a stalled RNA polymerase II mechanism

Project description:Transcription of immediate early genes (IEGs) in neurons is exquisitely sensitive to neuronal activity, but the mechanism underlying the earliest of these transcription events is largely unknown. Here we demonstrate that very fast IEGs (VF-IEGs) such as arc/arg3.1 are poised for rapid transcription by the stalling of RNA Polymerase II (Pol II) just downstream of the transcription start site. RNAi-depletion of two subunits of Negative Elongation Factor, a mediator of Pol II stalling, reduces the Pol II occupancy of the arc promoter and compromises the rapid induction of arc and other VF-IEGs. In contrast, reduction of Pol II stalling did not prevent expression of fast IEGs (F-IEGs). These F-IEGs are expressed with comparatively slower kinetics and largely lack promoter proximal Pol II stalling. Taken together, our data strongly indicate that very fast kinetics of neuronal IEG expression require poised Pol II and suggest a role for this mechanism in transcription-dependent learning and memory. Examination of Pol II bindnig genome-wide in rat neurons

2011-05-24 | E-GEOD-22878 | biostudies-arrayexpress

Neurotoxin tetrodotoxin TTX withdrawal induced neuronal activity: RNA Pol II is poised for rapid induction of arc and other neuronal VF-IEGs

Project description:Transcription of immediate early genes (IEGs) in neurons is exquisitely sensitive to neuronal activity, but the mechanism underlying the earliest of these transcription events is largely unknown. Here we demonstrate that very fast IEGs (VF-IEGs) such as arc/arg3.1 are poised for rapid transcription by the stalling of RNA Polymerase II (Pol II) just downstream of the transcription start site. RNAi-depletion of two subunits of a mediator of Pol II stalling, Negative Elongation Factor, reduces Pol II occupancy of the arc promoter and compromises rapid induction of arc and other VF-IEGs. In contrast, reduction of Pol II stalling did not prevent expression of other fast IEGs (F-IEGs). These F-IEGs are expressed with comparatively slower kinetics and largely lack promoter proximal Pol II stalling. Taken together, our data strongly indicate that very fast kinetics of neuronal IEG expression require poised Pol II and suggest a role for this mechanism in transcription-dependent learning and memory.

2011-04-15 | GSE22622 | GEO

Neurotoxin tetrodotoxin TTX withdrawal induced neuronal activity: RNA Pol II is poised for rapid induction of arc and other neuronal VF-IEGs

Project description:Transcription of immediate early genes (IEGs) in neurons is exquisitely sensitive to neuronal activity, but the mechanism underlying the earliest of these transcription events is largely unknown. Here we demonstrate that very fast IEGs (VF-IEGs) such as arc/arg3.1 are poised for rapid transcription by the stalling of RNA Polymerase II (Pol II) just downstream of the transcription start site. RNAi-depletion of two subunits of a mediator of Pol II stalling, Negative Elongation Factor, reduces Pol II occupancy of the arc promoter and compromises rapid induction of arc and other VF-IEGs. In contrast, reduction of Pol II stalling did not prevent expression of other fast IEGs (F-IEGs). These F-IEGs are expressed with comparatively slower kinetics and largely lack promoter proximal Pol II stalling. Taken together, our data strongly indicate that very fast kinetics of neuronal IEG expression require poised Pol II and suggest a role for this mechanism in transcription-dependent learning and memory. TTX withdrawal induced neuronal activity. To study activity-induced gene expression, neurons were treated with TTX for 48 hours and then TTX was washed out either for 15 minutes (W15) or for 45 minutes (W45). Gene expression was measured in these two groups in comparison to TTX treated neurons.

2011-04-14 | E-GEOD-22622 | biostudies-arrayexpress

Rapid transcription of arc/arg3.1 and other very fast immediate early genes in response to neuronal activity is mediated by a stalled RNA polymerase II mechanism

2011-05-24 | GSE22878 | 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