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SRP013290
Drosophila melanogaster
1 Downloadable Sample
Illumina Genome Analyzer II
Description
In animals, the piRNA pathway preserves the integrity of gametic genomes, guarding them against the activity of mobile genetic elements. This innate immune mechanism relies on distinct genomic loci, termed piRNA clusters, to provide a molecular definition of transposons, enabling their discrimination from genes. piRNA clusters give rise to long, single-stranded precursors which are processed into primary piRNAs through an unknown mechanism. These can engage in an adaptive amplification loop, the ping-pong cycle, to optimize the content of small RNA populations via the generation of secondary piRNAs. Many proteins have been ascribed functions in either primary biogenesis or the ping-pong cycle, though for the most part the molecular functions of proteins implicated in these pathways remain obscure. Here, we link shutdown, a gene previously shown to be required for fertility in Drosophila, to the piRNA pathway. Analysis of knockdown phenotypes in both the germline and somatic compartments of the ovary demonstrate important roles for shutdown in both primary biogenesis and the ping-pong cycle. shutdown is a member of the FKBP family of immunophilins. Shu contains domains implicated in peptidyl-prolyl cis-trans isomerase activity and in the binding of HSP90-family chaperones, though the relevance of these domains to piRNA biogenesis is unknown. Overall design: Analysis of mRNA expression in Drosophila OSS cells transfected with GFP dsRNA. One sample and replicate, used to establish the OSS baseline transcriptome in the presence of exogenous RNAi activity.
Publication Title
shutdown is a component of the Drosophila piRNA biogenesis machinery.
Sample Metadata Fields
Specimen part, Subject
View Samples- Drosophila melanogaster
- 10 Downloadable Samples
Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Drosophila H1 regulates the genetic activity of heterochromatin by recruitment of Su(var)3-9.
Sample Metadata Fields
Specimen part
View Samples- Drosophila melanogaster
- 10 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Indicated cells were subjected to RNAi against linker histone H1, Nautilus (control), or GFP (control). RNA was isolated and subjected to Affymetrix GeneChIP Drosophila Genome 2.0 arrays
Publication Title
Drosophila H1 regulates the genetic activity of heterochromatin by recruitment of Su(var)3-9.
Sample Metadata Fields
Specimen part
View Samples- Drosophila melanogaster
- 8 Downloadable Samples
- Illumina Genome Analyzer II
Description
Combining RNAi in cultured cells and analysis of mutant animals, we probed roles of known piRNA pathway components in the initiation and effector phases of transposon silencing. Overall design: total RNA and RNA associated with Piwi was isolated and size-fractionated by PAGE into 19-29nt. These were processed and sequenced on Illumina Genome Analyzer II.
Publication Title
Probing the initiation and effector phases of the somatic piRNA pathway in Drosophila.
Sample Metadata Fields
Specimen part, Subject
View Samples- Drosophila melanogaster
- 4 Downloadable Samples
- Illumina Genome Analyzer II
Description
Salivary glands or larval ovaries were isolated from transgenic flies expressing RNAi targeting Nautilus (control) or linker histone H1 using a Tub-Gal4 driver. Overall design: ~200 larvae were used to isolate salivary glands or ovaries, independently. Total RNA was isolated using Trizol reagent following manufacturer''s guidelines. Then 5 µg of total RNA was separated on a polyacrylamide gel, and 18-29 nt small RNAs were isolated for cloning.
Publication Title
Drosophila H1 regulates the genetic activity of heterochromatin by recruitment of Su(var)3-9.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Viruses lack the basic machinery needed to replicate and therefore must hijack host metabolism to propagate. Virus-induced metabolic alterations have yet to be systematically studied in the context of the host transcriptional regulation, offering insight into host-pathogen metabolic interplay. In this work we identified Hepatitis C Virus (HCV)-responsive regulators by coupling system-wide metabolic flux analysis with targeted perturbation of nuclear receptors in primary human hepatocytes. We find HCV-induced up-regulation of glycolysis, ketogenesis and drug metabolism, controlled by activation of HNF4, PPAR, FXR and PXR, respectively. Pharmaceutical inhibition of HNF4 reversed HCV-induced glycolysis, blocking viral replication while increasing apoptosis in infected cells showing a viral-induced dependence on glycolysis. In contrast, pharmaceutical inhibition of PPAR or FXR reversed HCV-induced ketogenesis, but increased viral replication demonstrating a unique host anti-viral response. Our results show that viral-induced changes to host metabolism can be detrimental to its lifecycle demonstrating a distinct biological complexity.
Publication Title
Nuclear receptors control pro-viral and antiviral metabolic responses to hepatitis C virus infection.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 22 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
To investigate the role of YAP/TAZ as b-catenin inhibitors, we compared the expression profiles of Rex1GFPd2 ES cells transfected with siControl#1, siControl#2, siYAP/TAZ#1, siYAP/TAZ#2 and cultured in 2i medium or PD-only medium
Publication Title
YAP/TAZ incorporation in the β-catenin destruction complex orchestrates the Wnt response.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 16 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
TGF ligands act as tumor suppressors in early stage tumors but are paradoxically diverted into potent prometastatic factors in advanced cancers. The molecular nature of this switch remains enigmatic. We now show that TGF-dependent cell migration, invasion and metastasis are empowered by mutant-p53.
Publication Title
A Mutant-p53/Smad complex opposes p63 to empower TGFbeta-induced metastasis.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 38 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Aerobic glycolysis tunes YAP/TAZ transcriptional activity.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 14 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Reprogramming of cancer cell metabolism toward aerobic glycolysis, i.e. the Warburg effect, is a hallmark of cancer; according to current views, the rationale for selecting such energy-inefficient metabolism is the need to increase cellular biomass to sustain production of daughter cells and proliferation. In this view, metabolic reprogramming is considered as a simple phenotypic endpoint that occurs as a consequence of signal transduction mechanisms, including oncogene-driven nutrient uptake and metabolic rewiring. A newly emerging paradigm is instead that transcriptional networks and oncogenic signaling can also be regulated downstream of metabolic pathways, that assume causative roles in controlling cancer cell behavior, above and beyond their core biochemical function. To explore possible links between glucose metabolism and nuclear gene transcription we compared immortalized mammary epithelial cells (MCF10A) and metastatic breast cancer cells (MDA-MB-231) growing in high glucose or in the presence of a widely used inhibitor of glucose uptake / glucose metabolism, 2-deoxy-glucose (2DG).
Publication Title
Aerobic glycolysis tunes YAP/TAZ transcriptional activity.
Sample Metadata Fields
Cell line, Treatment
View Samples