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SRP061537
Mus musculus
18 Downloadable Samples
Illumina HiSeq 2000, Illumina Genome Analyzer IIx, Illumina HiSeq 1000, Illumina Genome Analyzer II
Description
We report cell type specific Nova HITS-CLIP using BAC-transgenic lines expressing GFP-Nova under the motor neuron specific choline acetyltransferase (Chat) promoter. By comparing transcriptome wide Nova binding map in motor neurons and that in the whole spinal cord, we identified differential Nova binding sites in motor neurons, which correlate with motor neuron specific RNA processing. Overall design: 14 total samples were analyzed. For HITS-CLIP, 4 biological replicates were performed for each BAC-transgenic line, as well as the whole spinal cord. For RNA-seq, 2 biological repliates were performed on the whole spinal cord.
Publication Title
Cell type-specific CLIP reveals that NOVA regulates cytoskeleton interactions in motoneurons.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 24 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
FMRP stalls ribosomal translocation on mRNAs linked to synaptic function and autism.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 24 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The Fragile X Mental Retardation Protein, FMRP, is thought to regulate the translation of a specific set of neuronal mRNAs on polyribosomes. Therefore, we prepared polyribosomes on sucrose gradients and purified mRNA specifically from these fractions, as well as the total mRNA levels, to determine whether a set of mRNAs might be changed in its % association with polyribosomes in the absence of FMRP in the KO mouse model.
Publication Title
FMRP stalls ribosomal translocation on mRNAs linked to synaptic function and autism.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 34 Downloadable Samples
- Illumina HiSeq 2500
Description
Limitation for amino acids is thought to regulate translation in mammalian cells primarily by signaling through the kinases mTORC1 and GCN2. We find that limitation for the amino acid arginine causes a selective loss of tRNA charging, which regulates translation through ribosome pausing at two of six arginine codons. Interestingly, limitation for leucine, an essential and abundant amino acid in protein, results in little or no ribosome pausing. Chemical and genetic perturbation of mTORC1 and GCN2 signaling revealed that their robust response to leucine limitation prevents ribosome pausing, while an insufficient response to arginine limitation led to loss of arginine tRNA charging and ribosome pausing. Codon-specific ribosome pausing decreased protein production and triggered premature ribosome termination without significantly reducing mRNA levels. Together, our results suggest that amino acids which are not optimally sensed by the mTORC1 and GCN2 pathways still regulate translation through an evolutionarily conserved mechanism based on synonymous codon usage. Overall design: Ribosome profiling was performed in HEK293T, HCT116, or HeLa cells during limitation for leucine or arginine for 3 or 6 hours to determine the effect of limiting single amino acid levels of ribosome elongation kinetics at the cognate codons. The same cell lines grown in nutrient-rich conditions were used as a control. These experiments were repeated in HEK293T cells with 250 nM Torin1, in cells stably expressing a flag-tagged wild-type or Q99L mutant RagB-GTPase or hrGFP, and in a GCN2 knockout cell line to determine the role of the mTORC1 and GCN2 pathways.
Publication Title
Translational Control through Differential Ribosome Pausing during Amino Acid Limitation in Mammalian Cells.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens, Rattus norvegicus
- 22 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
[Hela cells]: We performed cdr2 knockdown with a pool of 4 cdr2-specific siRNAs to test whether cdr2 may regulate c-myc target genes as cells passage through mitosis.
Publication Title
The onconeural antigen cdr2 is a novel APC/C target that acts in mitosis to regulate c-myc target genes in mammalian tumor cells.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
Inhibition of Brd4 with Jq1 in neurons with or without BDNF stimulation Overall design: Examination of the effects of Jq1 treatment on primary mouse cortical neurons
Publication Title
BET protein Brd4 activates transcription in neurons and BET inhibitor Jq1 blocks memory in mice.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 18 Downloadable Samples
- NextSeq 500
Description
Widespread epigenetic disruptions in FXS mice leads to transcriptional changes that likely contribute to the neuronal phenotpyes underlying FXS. Overall design: 7DIV cultured cortical neurons from WT or Fmr1 KO mice were treated for 24 hours with vehicle, Jq1, or THZ, performed in triplicate.
Publication Title
Excess Translation of Epigenetic Regulators Contributes to Fragile X Syndrome and Is Alleviated by Brd4 Inhibition.
Sample Metadata Fields
Treatment, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Transcriptome-wide miR-155 binding map reveals widespread noncanonical microRNA targeting.
Sample Metadata Fields
Specimen part
View Samples- Rattus norvegicus
- 9 Downloadable Samples
- Illumina HiSeq 2500
Description
How type I / II interferons (IFNs) prevent periodic re-emergence of latent pathogens in tissues of diverse cell-types remains unknown. Using homogenous neuron cultures latently-infected with herpes simplex virus (HSV), we show that extrinsic type I or II IFN act directly on neurons to induce unique gene expression signatures and inhibit the reactivation-specific burst of viral genome-wide transcription called Phase I. Surprisingly, IFNs suppressed reactivation only during a limited period early in Phase I preceding productive virus growth. Sensitivity to type II IFN was selectively lost if viral ICP0, which normally accumulates later in Phase I, was expressed prior to reactivation. Thus, IFNs suppress reactivation by preventing initial expression of latent genomes but are ineffective once Phase I viral proteins accumulate and limit IFN action. This demonstrates that inducible reactivation from latency is only transiently sensitive to IFNs. Moreover, it illustrates how latent pathogens escape host immune control to periodically replicate by rapidly deploying an interferon-resistant state. Overall design: Superior cervical ganglia (SCG) neuron cultures harboring reactivating HSV-1 treated with IFNb or IFNg. Neurons were harvested for RNA 20h after reactivation (in the presence or absence of IFN) for RNA-seq. Libraries were generated following Illumina Truseq Ribo-Zero protocol.
Publication Title
Immune Escape via a Transient Gene Expression Program Enables Productive Replication of a Latent Pathogen.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
microRNAs (miRNAs) are essential components of gene regulation, but identification of miRNA targets remains a major challenge. Most target prediction and discovery relies on perfect complementarity of the miRNA seed to the 3 untranslated region (UTR). However, it is unclear to what extent miRNAs target sites without seed matches. Here, we performed a transcriptome-wide identification of the endogenous targets of a single miRNAmiR-155in a genetically controlled manner. We found that approximately forty percent of miR-155-dependent Argonaute binding occurs at sites without perfect seed matches. The majority of these non-canonical sites feature extensive complementarity to the miRNA seed with one mismatch. These non-canonical sites confer regulation of gene expression albeit less potently than canonical sites. Thus, non-canonical miRNA binding sites are widespread, often contain seed-like motifs, and can regulate gene expression, generating a continuum of targeting and regulation.
Publication Title
Transcriptome-wide miR-155 binding map reveals widespread noncanonical microRNA targeting.
Sample Metadata Fields
Specimen part
View Samples