Filters
Technology
Platform
SRP001010
Caenorhabditis elegans
11 Downloadable Samples
Illumina Genome Analyzer
Description
While the genome sequence of many animals is now complete, their transcriptomes are less well characterised. Both genome-scale tiling arrays and massively parallel sequencing now allow transcriptomes to be mapped at unprecedented depth. We used both technologies to map the C. elegans transcriptome across development. This unbiased overview can serve as a framework for assessing transcriptome changes in a mutant animal and we compared the wild-type data with that of animals that have lost the nonsense-mediated decay (NMD) pathway. Results We find that while the great majority of detectable transcripts map to known gene structures, over 5% of transcribed regions are novel, falling outside current gene annotations. We show that at least 40% of these are novel exons. We also used both technologies to assess isoform complexity and estimate that at least 17% of genes change their major isoform across development. Having mapped the wild-type transcriptome, we examined how this is perturbed in animals lacking nonsense -mediated decay (NMD). NMD prevents expression of prematurely truncated proteins by degrading transcripts containing premature termination codons (PTCs). We find that ~20% of all genes produce transcripts that appear to be targets for NMD. While most of these arise from splicing errors, NMD targets are also enriched for transcripts that contain short open reading frames upstream of the predicted translational start (uORFs). We find an intriguing relationship between the strength of Kozak consensus surrounding the true start codon and the degree to which these uORF containing transcripts are targeted by NMD, suggesting that translational efficiency may be coupled to transcript turnover via the NMD pathway for many transcripts. Conclusions We have generated a high-resolution map of the C. elegans transcriptome and have used it to identify transcripts that are endogenous targets of the NMD machinery. We find that these targets arise principally through splicing errors and suggest that splicing and NMD are highly interlinked processes.
Publication Title
High resolution transcriptome maps for wild-type and nonsense-mediated decay-defective Caenorhabditis elegans.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 506 Downloadable Samples
- Illumina HiSeq 2000
Description
The study examined early transcriptional changes in the brain of different mouse models of spinocerebellar ataxia type 3, a dominantly-inherited neurodegenerative disease caused by a CAG repeat expansion in the ATXN3 gene. The goal was to identify early transcriptional signatures that are strongly associated with the accumulation and aggregation of the disease protein, ataxin-3, in the brain. The study also investigated the extent to which the observed transcriptional changes might be contributors to disease pathogenesis. Overall design: The overall study includes multiple different RNA-seq runs utilizing wild-type, two different knock-in mouse models of SCA3 (a traditional and variant), two different transgenic models of SCA3 (Q84 and Q15), and an ataxin-3 knock-out mouse. In total, 19 wild-type mice, 13 homozygous variant knock-in mice, 6 heterozygous variant knock-in mice, 4 traditional homozygous knock-in mice, 4 traditional heterozygous knock-in mice, 4 Q84 transgenic mice, 4 Q15 transgenic mice, and 3 ataxin-3 knock-out mice. The majority of the study examined the pons of the mice, and with one smaller run examining the deep cerebellar nuclei of wild-type and variant homozygous knock-in mice (n=3 each).
Publication Title
Comparison of spinocerebellar ataxia type 3 mouse models identifies early gain-of-function, cell-autonomous transcriptional changes in oligodendrocytes.
Sample Metadata Fields
Cell line, Subject
View Samples- Homo sapiens
- 11 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Background: The basic helix-loop-helix transcription factor TWIST1 (Twist) is involved in embryonic cell lineage determination and mesodermal differentiation. There is evidence to indicate that Twist expression plays a role in breast tumor formation and metastasis, but the role of Twist in dysregulating pathways that drive the metastatic cascade is unclear. Importantly, the genes and pathways dysregulated by Twist in cell lines and mouse models have not been validated against data obtained from patient samples.
Publication Title
Genomic pathways modulated by Twist in breast cancer.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Illumina Genome Analyzer
Description
Many animal species employ a chromosome-based mechanism of sex determination, which has led to coordinate evolution of dosage compensation systems. Dosage compensation not only corrects the imbalance in the number of X-chromosomes between the sexes, but is also hypothesized to correct dosage imbalance within cells due to mono-allelic X expression and bi-allelic autosomal expression, by upregulating X-linked genes (termed â??Ohnoâ??s hypothesisâ??). Although this hypothesis is well supported by expression analyses of individual X-linked genes and by array-based transcriptome analyses, a recent study claimed that no such X upregulation exists in mammals and C. elegans based on RNA-sequencing and proteomics analyses. We provide RNA-seq RNA-seq analysis of mouse female PGK12.1 ES cells with two active X chromosomes and confirmed that the X chromosome is upregulated, consistent with the previous microarray study. Overall design: Examination of expression of X-linked and autosomal genes in mouse female ES cells with two active X chromosomes.
Publication Title
Bipartite structure of the inactive mouse X chromosome.
Sample Metadata Fields
Sex, Cell line, Subject
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Gene 2.0 ST Array (hugene20st), Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
LASP-1: a nuclear hub for the UHRF1-DNMT1-G9a-Snail1 complex.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Oryza sativa
- 12 Downloadable Samples
- Affymetrix Rice Genome Array (rice)
Description
Leaves and panicles from recurrent parent KMR3 and a high yielding KMR3-O.rufipogon introgression line were used
Publication Title
Os11Gsk gene from a wild rice, Oryza rufipogon improves yield in rice.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Nuclear LASP-1 has a direct correlation with the overall survival of breast cancer patients. Gene expression analysis of MCF7 human breast cancer cells cultured in 3D-Matrigel was performed.
Publication Title
LASP-1: a nuclear hub for the UHRF1-DNMT1-G9a-Snail1 complex.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Bos taurus
- 6 Downloadable Samples
- Affymetrix Bovine Genome Array (bovine)
Description
Bovine articular chondrocytes were grown in micromass culture and were either untreated or treated with 5 ng TGF-b1/ml for 8 hours to identify genes regulated by TGF-b.
Publication Title
Altered responsiveness to TGF-β results in reduced Papss2 expression and alterations in the biomechanical properties of mouse articular cartilage.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
We used microarrays to study the effect of Chd1 loss of function in mouse ES cells.
Publication Title
Chd1 regulates open chromatin and pluripotency of embryonic stem cells.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Nod2 has been extensively characterized as a bacterial sensor that induces an antimicrobial and inflammatory gene expression program. Therefore, it is unclear why Nod2 mutations that disrupt bacterial recognition are paradoxically among the highest risk factors for Crohns disease, which involves an exaggerated immune response directed at intestinal bacteria. Previous studies from our lab have shown that mice deficient in Atg16L1, another Crohns disease susceptibility gene, develop abnormalities in Paneth cells, specialized epithelial cells in the small intestine involved in antimicrobial responses.
Publication Title
Bacterial sensor Nod2 prevents inflammation of the small intestine by restricting the expansion of the commensal Bacteroides vulgatus.
Sample Metadata Fields
Age, Specimen part
View Samples