Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

QuaNCAT analysis comparing proteins synthesized in neurites and soma in ASCL1-iNeurons

ABSTRACT: Local translation in ASCL1-iNeurons was probed using QuaNCAT

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Embryonic Stem Cell

SUBMITTER: Erik McShane

LAB HEAD: Marina Chekulaeva

PROVIDER: PXD005059 | Pride | 2018-10-17

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	MaxQuant_Output.zip	Other
	Statler_20160907_SEM_David_One_2h.raw	Raw
	Statler_20160907_SEM_David_One_4h.raw	Raw
	Statler_20160907_SEM_David_Two_2h.raw	Raw
	Statler_20160907_SEM_David_Two_4h.raw	Raw

Items per page:

1 - 5 of 6

Publications

RNA localization is a key determinant of neurite-enriched proteome.

Zappulo Alessandra A van den Bruck David D Ciolli Mattioli Camilla C Franke Vedran V Imami Koshi K McShane Erik E Moreno-Estelles Mireia M Calviello Lorenzo L Filipchyk Andrei A Peguero-Sanchez Esteban E Müller Thomas T Woehler Andrew A Birchmeier Carmen C Merino Enrique E Rajewsky Nikolaus N Ohler Uwe U Mazzoni Esteban O EO Selbach Matthias M Akalin Altuna A Chekulaeva Marina M

Nature communications 20170919 1

Protein subcellular localization is fundamental to the establishment of the body axis, cell migration, synaptic plasticity, and a vast range of other biological processes. Protein localization occurs through three mechanisms: protein transport, mRNA localization, and local translation. However, the relative contribution of each process to neuronal polarity remains unknown. Using neurons differentiated from mouse embryonic stem cells, we analyze protein and RNA expression and translation rates in ...[more]

PMID: 28928394

Similar Datasets

RNA-seq of neuronal compartments with perturbed mRNA degradation machinery

Project description:We have perturbed mRNA degradation machinery and investigated the change in subcellular localization of mRNA in Ascl1-induced neurons (iNeurons). Mutant iNeuron line harbouring a ponasteroneA-inducible heterozygous dominant-negative Caf1 (dnCaf1) was generated, separated into neuronal compartments (soma and neurites) and sequenced in parallel with compartments from the Wild Type iNeurons (WT). Differential localization of mRNA between soma and neurites in the WT was then compared to the localization in dnCaf1 in order to identify the changes in localization.

2023-12-31 | E-MTAB-9398 | biostudies-arrayexpress

Slamseq of subcellular compartments in neurons

Project description:We performed a SLAMseq Metabolic RNA Labeling on neuronal subcellular compartments, e.g. neurites and soma, derived from Ascl1-induced neurons (iNeurons). This experimental approach provides a snapshot of mRNA kinetics which allows to estimate the half-lives of mRNAs. These data was used to investigate the influence of mRNA degradation machinery in both neuronal compartments.

2023-07-12 | E-MTAB-9400 | biostudies-arrayexpress

Depletion of m6A methylation by conditional Mettl3 knockout in Ascl1-induced neurons

Project description:We have perturbed RNA methylation machinery and investigated the change in subcellular localization of mRNA in Ascl1-induced neurons (iNeurons). Mutant iNeuron line harbouring tagged endogenous Mettl3 was generated which allowed for the selective and targeted depletion of Mettl3 protein with the addition of dTAG. Cells were treated with dTAG for 40 hours then separated into compartments (neurites and soma) and then sequenced in parallel with samples which received no dTAG treatment.

2023-07-12 | E-MTAB-9643 | biostudies-arrayexpress

m6A-RIP-seq of Ascl1-induced neurons.

Project description:We performed m6A-RIPs in Ascl1-induced neurons (iNeurons) to investigate the neuronal m6A epitranscriptome. Immunoprecipitation was done twice using two different antibodies, acquired from Abcam and Synaptic Systems (SySy), allowing for a more robust detection of m6A modification marks. Additionally, RIP-seq was performed separately with intact and fragmented RNA. The former approach allowed to identify proportions of m6A-modified transcripts among the total number, while the latter approach provided the information to identify genomic coordinates of m6A peaks.

2023-07-12 | E-MTAB-9542 | biostudies-arrayexpress

Slamseq of whole neurons with perturbed mRNA degradation machinery

Project description:We perturbed mRNA degradation machinery in Ascl1-induced neurons (iNeurons) and investigated the change in mRNA half-lives. We performed SLAMseq Metabolic RNA Labeling on Mutant iNeuron line harbouring a ponasteroneA-inducible heterozygous dominant-negative Caf1 (dnCaf1) and on Wild Type iNeurons (WT). The Slamseq technique provided snapshots of mRNA kinetics allowing to estimate mRNA half-lives and assess the effect of mRNA degradation machinery on the level of mRNA stability.

2023-07-12 | E-MTAB-9545 | biostudies-arrayexpress

hnRNP R Knock-out affects the axonal and somatic proteome

Project description:We grew neurons in microchambers to separate axons and soma in different compartments which could be independently harvested for proteomic analysis. Using this model system, we studied the effect of the knock-out of hnRNP R on the axonal and somatic proteome.

2024-08-22 | PXD038368 | Pride

mRNA-Seq of neuronal compartments in shRNA-mediated knockdown of Larp1 in mouse primary cortical neurons

Project description:To study the effect of Larp1 on the abundance and subcellular localization of 5'TOP containing mRNAs, Larp1 was depleted from mouse primary cortical neurons using shRNAs. RNA from subcellular compartments (neurite and soma cytoplasm) was isolated and sequenced in parallel with scrambled control shRNA expressing samples.

2023-07-12 | E-MTAB-12886 | biostudies-arrayexpress

mRNA-Seq of neuronal compartments with perturbed mRNA degradation machinery (overexpression of dnCaf1) in mouse primary cortical neurons

Project description:To study the correlation between mRNA stability and subcellular mRNA localisation we globally interferred with mRNA degradation in primary cortical neurons by overexpressing a catalytic mutant of deadenylase CAF1 that functions as a dominant negative form. Neurons were separated into subcellular compartments (neurite, soma-cytoplasm and nucleus) and sequenced in parallel with respective compartments from GFP- expressing control neuons.

2023-07-12 | E-MTAB-12887 | biostudies-arrayexpress

Functionally diverse dendritic mRNAs rapidly associate with ribosomes following a novel experience

Project description:The subcellular localization and translation of messenger RNA (mRNA) supports functional differentiation between cellular compartments. In neuronal dendrites, local translation of mRNA provides a rapid and specific mechanism for synaptic plasticity and memory formation, and might be involved in the pathophysiology of certain brain disorders. Despite the importance of dendritic mRNA translation, little is known about which mRNAs can be translated in dendrites in vivo and when their translation occurs. Here we collect ribosome-bound mRNA from the dendrites of CA1 pyramidal neurons in the adult mouse hippocampus. We find that dendritic mRNA rapidly associates with ribosomes following a novel experience consisting of a contextual fear conditioning trial. High throughput RNA sequencing followed by machine learning classification reveals an unexpected breadth of ribosome-bound dendritic mRNAs, including mRNAs expected to be entirely somatic. Our findings are in agreement with a mechanism of synaptic plasticity that engages the acute local translation of functionally diverse dendritic mRNAs. RNA-Seq of ribosome-bound mRNA immunoprecipitated from dendrites and soma of CA1 pyramidal neurons in the mouse hippocampus

2014-07-30 | E-GEOD-58343 | biostudies-arrayexpress

ASCL1: a pioneer factor that induces subtype switching and characterizes adrenergic neuroblastoma

Project description:Neuroblastoma is an embryonic malignancy originating from early nerve cells. Neuroblastoma retains plasticity, interconverting between the mesenchymal (MES) and adrenergic (ADRN) states, which are controlled by different sets of transcription factors forming the core regulatory circuit (CRC). However, their functional roles and cooperative mechanisms in neuroblastoma pathogenesis are poorly understood. Here, we demonstrate that overexpression of ASCL1 in MES neuroblastoma cells opens closed chromatin at the promoters of key ADRN genes, accompanied by epigenetic activation and establishment of enhancer-promoter interactions, thereby initiating subtype switching. ASCL1 inhibits the TGFb-SMAD2/3 pathway but activates the BMP-SMAD1-ID3/4 pathway, serving as negative feedback to balance the function of ASCL1-TCF12 dimers. ASCL1 and other ADRN CRC members potentiate each other’s activity, increasing the expression of the original targets and inducing a new set of genes, thereby promoting conversion to ADRN neuroblastoma. Thus, via its pioneer factor function, ASCL1 serves as a master regulator that characterizes ADRN neuroblastoma.

2023-12-08 | PXD037670 | Pride