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SRP018838
Homo sapiens
62 Downloadable Samples
IlluminaHiSeq2000
Description
RNA-seq transcriptome measurements are typically performed by isolating RNA from large numbers of cells in culture or tissues. While highly informative, such experiments mask the variability in gene expression patterns that exists between individual cells. To gain insight into the dynamics of gene expression on the level of single-cells, we have carried out the transcriptomes of single-cells from the GM12878 cell line using RNA-seq. Overall design: Single GM12878 cells were picked and RNA-seq libraries were generated using the SMART-seq protocol. We also carried out RNA-seq experiments on pools of 10, 30 and 100 cells, on 100pg and 10ng of total RNA, and on pools of 10 cells that were subsequently split into 10 separate sample and processed as if they were single cells in order to assess technical variation in our experiments.
Publication Title
From single-cell to cell-pool transcriptomes: stochasticity in gene expression and RNA splicing.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 119 Downloadable Samples
- Illumina HiSeq 2500, Illumina HiSeq 2000
Description
We report the application of single-cell and bulk RNA sequencing technology to examine the noncoding transcriptome of cells undergoing reprogramming to the pluripotent state. Overall design: Examination of noncoding RNAs in reprogrammming cells. We examined iPS cells grown in standard ES cell culture conditions, as well as iPS cells grown in "2i" conditions (small molecule inhibition of Mek and Gsk3). We also compared our iPS samples to male and female ES cells (mES, fES).
Publication Title
Single-cell transcriptome analysis reveals dynamic changes in lncRNA expression during reprogramming.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina HiSeq 2500
Description
The innate inflammatory response must be tightly regulated to ensure effective immune protection while avoiding inflammation-related pathologies. The transcription factor NF-kB is a critical mediator of the inflammatory response, and its dysregulation has been associated with immune related malignancies. We herein show that miR-155, miR-146a and NF-kB form a regulatory network that tunes the macrophage inflammatory response in mice. We show that elevated miR-155 expression potentiates NF-kB activity in miR-146a deficient mice, thus leading to an overactive acute inflammatory response and chronic inflammation. Enforced miR-155 expression overrides miR-146a-mediated repression of NF-kB activation, thus emphasizing that miR-155 plays a dominant, downstream role in promoting inflammation. We further show that miR-155 deficient macrophages exhibit a suboptimal inflammatory response when exposed to low levels of inflammatory stimuli. Importantly, we demonstrate a temporal asymmetry between miR-155 and miR-146a expression during macrophage activation, which forms a combined positive and negative feedback network on NF-kB activity. This miRNA based regulatory network enables a robust and time-limited inflammatory response essential for functional immunity. Overall design: RNA-seq of wild-type and microRNA-146/155 knock-out bone marrow derived macrophages after LPS stimulation
Publication Title
An NF-κB-microRNA regulatory network tunes macrophage inflammatory responses.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina HiSeq 2000
Description
MicroRNAs have emerged as key regulators of B cell fate decisions and immune function. Deregulation of several microRNAs in B cells leads to the development of autoimmune disease and cancer in mice. We demonstrate that the microRNA-212/132 cluster (miR-212/132) is induced in B cells in response to B cell receptor signaling. Enforced expression of miR-132 results in a block in early B cell development at the pre-pro-B cell to pro-B cell transition and induces apoptosis in primary bone marrow B cells. Importantly, loss of miR-212/132 results in increased B cell output under non-homeostatic conditions. We find that miR-212/132 regulates B lymphopoiesis by targeting the transcription factor SOX4. Co-expression of SOX4 with miR-132 rescues the defect in B cell development from over-expression of miR-132 alone. In addition, we show that the expression of miR-132 in cells that are prone to spontaneous B cell cancers can have a protective effect on cancer development. We have thus uncovered a novel regulator of B cell lineage specification that may potential applications in B cell cancer therapy Overall design: RNA-seq of wild-type and microRNA-212/132 knock-out B-cells after IgM stimulation
Publication Title
The microRNA-212/132 cluster regulates B cell development by targeting Sox4.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 147 Downloadable Samples
Illumina HumanHT-12 V4.0 expression beadchip
Description
The disrupted genetic mechanisms underlying neural abnormalities in Autism Spectrum Disorder remain mostly unknown and speculative. No biological marker nor genetic signature is currently available to assist with early diagnosis.
Publication Title
Prediction of autism by translation and immune/inflammation coexpressed genes in toddlers from pediatric community practices.
Sample Metadata Fields
Sex, Specimen part
View Samples- Drosophila melanogaster
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
Small non-coding RNAs that associate with Piwi proteins, called piRNAs, serve as guides for repression of diverse transposable elements in germ cells of Metazoa. In Drosophila, the genomic regions that give rise to piRNAs, the so-called piRNA clusters, are transcribed to generate long precursor molecules that are processed into mature piRNAs. How genomic regions that give rise to piRNA precursor transcripts are differentiated from the rest of the genome and how these transcripts are specifically channeled into the piRNA biogenesis pathway are not known. We found that trans-generationally inherited piRNAs provide the critical trigger for piRNA production from homologous genomic regions in the next generation by two different mechanisms. First, inherited piRNAs enhance processing of homologous transcripts into mature piRNAs by initiating the ping-pong cycle in the cytoplasm. Second, inherited piRNAs induce installment of the H3K9me3 mark on genomic piRNA cluster sequences. The HP1 homolog Rhino binds to the H3K9me3 mark through its chromodomain and is enriched over piRNA clusters. Rhino recruits the piRNA biogenesis factor Cutoff to piRNA clusters and is required for efficient transcription of piRNA precursors. We propose that trans-generationally inherited piRNAs act as an epigenetic memory for identification of substrates for piRNA biogenesis on two levels, by inducing a permissive chromatin environment for piRNA precursor synthesis and by enhancing processing of these precursors. Overall design: total RNA sequencing of RNA from ovaries of cuff+/- or cuff-/- flies
Publication Title
Transgenerationally inherited piRNAs trigger piRNA biogenesis by changing the chromatin of piRNA clusters and inducing precursor processing.
Sample Metadata Fields
Specimen part, Subject
View Samples- Drosophila melanogaster
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
Small non-coding RNAs that associate with Piwi proteins, called piRNAs, serve as guides for repression of diverse transposable elements in germ cells of Metazoa. In Drosophila, the genomic regions that give rise to piRNAs, the so-called piRNA clusters, are transcribed to generate long precursor molecules that are processed into mature piRNAs. How genomic regions that give rise to piRNA precursor transcripts are differentiated from the rest of the genome and how these transcripts are specifically channeled into the piRNA biogenesis pathway are not known. We found that trans-generationally inherited piRNAs provide the critical trigger for piRNA production from homologous genomic regions in the next generation by two different mechanisms. First, inherited piRNAs enhance processing of homologous transcripts into mature piRNAs by initiating the ping-pong cycle in the cytoplasm. Second, inherited piRNAs induce installment of the H3K9me3 mark on genomic piRNA cluster sequences. The HP1 homolog Rhino binds to the H3K9me3 mark through its chromodomain and is enriched over piRNA clusters. Rhino recruits the piRNA biogenesis factor Cutoff to piRNA clusters and is required for efficient transcription of piRNA precursors. We propose that trans-generationally inherited piRNAs act as an epigenetic memory for identification of substrates for piRNA biogenesis on two levels, by inducing a permissive chromatin environment for piRNA precursor synthesis and by enhancing processing of these precursors. Overall design: nuclear run-on in wildtype and Rhino knockdown to investigate the transcriptional activity in Rhino knockdown compared to wildtype
Publication Title
Transgenerationally inherited piRNAs trigger piRNA biogenesis by changing the chromatin of piRNA clusters and inducing precursor processing.
Sample Metadata Fields
Specimen part, Subject
View Samples- Drosophila melanogaster
- 2 Downloadable Samples
- Illumina HiSeq 2000
Description
Small non-coding RNAs that associate with Piwi proteins, called piRNAs, serve as guides for repression of diverse transposable elements in germ cells of Metazoa. In Drosophila, the genomic regions that give rise to piRNAs, the so-called piRNA clusters, are transcribed to generate long precursor molecules that are processed into mature piRNAs. How genomic regions that give rise to piRNA precursor transcripts are differentiated from the rest of the genome and how these transcripts are specifically channeled into the piRNA biogenesis pathway are not known. We found that trans-generationally inherited piRNAs provide the critical trigger for piRNA production from homologous genomic regions in the next generation by two different mechanisms. First, inherited piRNAs enhance processing of homologous transcripts into mature piRNAs by initiating the ping-pong cycle in the cytoplasm. Second, inherited piRNAs induce installment of the H3K9me3 mark on genomic piRNA cluster sequences. The HP1 homolog Rhino binds to the H3K9me3 mark through its chromodomain and is enriched over piRNA clusters. Rhino recruits the piRNA biogenesis factor Cutoff to piRNA clusters and is required for efficient transcription of piRNA precursors. We propose that trans-generationally inherited piRNAs act as an epigenetic memory for identification of substrates for piRNA biogenesis on two levels, by inducing a permissive chromatin environment for piRNA precursor synthesis and by enhancing processing of these precursors. Overall design: total RNA sequencing of RNA from ovaries of shWhite and Rhino knockdown flies
Publication Title
Transgenerationally inherited piRNAs trigger piRNA biogenesis by changing the chromatin of piRNA clusters and inducing precursor processing.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 32 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Infection of RAW264.7 cells for 24 hours with 32 Toxoplasma Progeny from a Type II x Type III cross
Publication Title
GRA25 is a novel virulence factor of Toxoplasma gondii and influences the host immune response.
Sample Metadata Fields
No sample metadata fields
View Samples- Anopheles gambiae
- 19 Downloadable Samples
- Affymetrix Plasmodium/Anopheles Genome Array (plasmodiumanopheles)
Description
Anopheles gambiae mosquitoes play an important role in malaria transmission. In sub-Saharan Africa, the dry season can last several months. The mechanisms for mosquito population to survive through the dry season are poorly understood. One possible mechanism is that adults increase their desiccation tolerance over the dry season. Genetic analyses have shown that inversions 2La, 2Rb, 2Rc, 2Rd and 2Ru are associated with aridity resistance, however little is known about the transcriptional response of genes in response to desiccation.
Publication Title
Genome-wide transcriptional analysis of genes associated with acute desiccation stress in Anopheles gambiae.
Sample Metadata Fields
Specimen part
View Samples