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SRP043008
Homo sapiens
39 Downloadable Samples
IlluminaHiSeq1000, IlluminaHiSeq1500
Description
The goal of this study is to simultaneously interrogate the gene expression programs in human host cells (human foreskin fibroblasts) infected with the intracellular parasite Trypanosoma cruzi. We conducted high-resolution sequencing of the transcriptomes of T. cruzi and infected human foreskin fibroblasts (HFFs) using an RNA-seq approach. An array of computational tools was applied to map reads to the T. cruzi and human genomes and reconstruct full-length transcripts. mRNA abundance was determined for T. cruzi genes at at various time points post-infection enabling us to identify co-expression patterns that correlate with the biology of the parasite. We also conducted a time course of infection in host cells to obtain a preliminary analysis of the dynamic nature of parasite and host cell gene expression programs in the context of infection. These data provide the first glimpse of T. cruzi gene expression programs that are uniquely activated in the context of intracellular infection along with the transcriptional response of the human host cell. The study provides a solid framework for future functional and genomic studies of Chagas disease as well as intracellular pathogenesis in general.
Publication Title
Transcriptome Remodeling in Trypanosoma cruzi and Human Cells during Intracellular Infection.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 58 Downloadable Samples
Affymetrix Human Genome U133A Array (hgu133a)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Integrated genomic analysis of colorectal cancer progression reveals activation of EGFR through demethylation of the EREG promoter.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 58 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Colorectal cancer (CRC) tumorigenesis proceedes through well defined clinical stages assoicated with charateristic mutations. To get a better understanding of CRC progression at the transcriptional level, we performed transcriptome profiling on samples from normal colonic tissues, pre-malignant adenomas, carcinomas and metatases.
Publication Title
Integrated genomic analysis of colorectal cancer progression reveals activation of EGFR through demethylation of the EREG promoter.
Sample Metadata Fields
Sex, Specimen part
View Samples- Arabidopsis thaliana
- 8 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Neonicotinoid insecticides control crop pests based on their action as agonists at the insect nicotinic acetylcholine receptor which accepts chloropyridinyl- and chlorothiazolyl- analogs almost equally well. In some cases, these compounds have also been reported to enhance plant vigor and (a)biotic stress tolerance, independent of their insecticidal function. However, this mode of action has not been specifically defined. Using Arabidopsis thaliana, we show that the neonicotinoid compounds, imidacloprid (IMI) and clothianidin (CLO), via their 6-chloropyridinyl-3-carboxylic acid and 2-chlorothiazolyl-5-carboxylic acid metabolites, respectively, induce salicylic acid (SA) associated plant responses. SA is a phytohormone best known for its role in plant defense against pathogens and as an inducer of systemic acquired resistance; however, it can also modulate abiotic stress responses. These neonicotinoids effect a similar global transcriptional response to that of SA including genes involved in (a)biotic stress response. Furthermore, similar to SA, IMI and CLO induce systemic acquired resistance resulting in reduced growth of a powdery mildew pathogen. The action of CLO induces the endogenous synthesis of SA via the SA biosynthetic enzyme ICS1, with ICS1 required for CLO-induced accumulation of SA, expression of the SA marker PR1, and fully enhanced resistance to powdery mildew. In contrast, the action of IMI does not induce endogenous synthesis of SA. Instead, IMI is further bioactivated to 6-chloro-2-hydroxypyridinyl-3-carboxylic acid, which is shown here to be a potent inducer of PR1 and inhibitor of SA-sensitive enzymes. Thus, via different mechanisms, these chloropyridinyl- and chlorothiazolyl- neonicotinoids induce SA responses associated with enhanced stress tolerance.
Publication Title
Neonicotinoid insecticides induce salicylate-associated plant defense responses.
Sample Metadata Fields
Age, Specimen part
View Samples