Gut microbes elicit specific changes in gene expression in the colon of mice. We colonized germ-free mice with microbial communities from the guts of humans, zebrafish and termites, human skin and tongue, soil and estuarine microbial mats.
Bacteria from diverse habitats colonize and compete in the mouse gut.
Sex, Specimen part
View SamplesWe profile gene expression changes in two mutant strains lacking the D. melanogaster HP1 homolog HP1B at the third instar larval stage. Compared to the yw control strain, several hundred genes are deregulated, with metabolic genes being over-represented among the deregulated gene set. Overall design: Examination of gene expression in two genotypes
HP1B is a euchromatic Drosophila HP1 homolog with links to metabolism.
Specimen part, Cell line, Subject
View SamplesRefined cancer models are required to assess the burgeoning number of potential targets for cancer therapeutics within a rapid and clinically relevant context. Here we utilize tumor-associated genetic pathways to transform primary human epithelial cells from epidermis, oropharynx, esophagus, and cervix into genetically defined tumors within an entirely human 3-dimensional (3-D) tissue environment incorporating cell-populated stroma and intact basement membrane (BM). These engineered organotypic tissues recapitulated natural features of tumor progression, including epithelial invasion through the BM, a complex process critically required for biologic malignancy in 90% of human cancers. Invasion was rapid, and potentiated by stromal cells. Oncogenic signals in 3-D tissue, but not 2-D culture, resembled gene expression profiles from spontaneous human cancers. Screening well-characterized signaling pathway inhibitors in 3-D organotypic neoplasia helped distil a clinically faithful cancer gene signature. Multi-tissue 3-D human tissue cancer models may provide an efficient and relevant complement to current approaches to characterize cancer progression.
Invasive three-dimensional organotypic neoplasia from multiple normal human epithelia.
No sample metadata fields
View SamplesRefined cancer models are required to assess the burgeoning number of potential targets for cancer therapeutics within a rapid and clinically relevant context. Here we utilize tumor-associated genetic pathways to transform primary human epithelial cells from epidermis, oropharynx, esophagus, and cervix into genetically defined tumors within an entirely human 3-dimensional (3-D) tissue environment incorporating cell-populated stroma and intact basement membrane (BM). These engineered organotypic tissues recapitulated natural features of tumor progression, including epithelial invasion through the BM, a complex process critically required for biologic malignancy in 90% of human cancers. Invasion was rapid, and potentiated by stromal cells. Oncogenic signals in 3-D tissue, but not 2-D culture, resembled gene expression profiles from spontaneous human cancers. Screening well-characterized signaling pathway inhibitors in 3-D organotypic neoplasia helped distil a clinically faithful cancer gene signature. Multi-tissue 3-D human tissue cancer models may provide an efficient and relevant complement to current approaches to characterize cancer progression.
Invasive three-dimensional organotypic neoplasia from multiple normal human epithelia.
Specimen part
View SamplesOncogenic Ras induces epidermal cell growth arrest. Induction of the JNK/Ap1 signaling cascade by expression of MKK7 overcomes Ras-induced cell growth arrest in a manner dependent on AP1 fucntion.
Tumor necrosis factor receptor 1/c-Jun-NH2-kinase signaling promotes human neoplasia.
No sample metadata fields
View SamplesMicroarray analysis was performed on retina/RPE/choroid samples taken from the right eyes of male chicks across control and recovery from form deprivation conditions.
Pathway analysis identifies altered mitochondrial metabolism, neurotransmission, structural pathways and complement cascade in retina/RPE/ choroid in chick model of form-deprivation myopia.
Sex, Specimen part, Treatment, Time
View SamplesBackground. Differential gene expression in adipose tissue during diet-induced weight loss followed by a weight stability period is not well characterized. Markers of these processes may provide a deeper understanding of the underlying mechanisms. Objective. To identify differentially expressed genes in human adipose tissue during weight loss and weight maintenance after weight loss. Design. RNA from subcutaneous abdominal adipose tissue from nine obese subjects was obtained and analyzed at baseline, after weight reduction on a low calorie diet (LCD), and after a period of group therapy in order to maintain weight stability. Results. Subjects lost 18.8 + 5.4% of their body weight during the LCD and maintained this weight during group therapy. Insulin sensitivity (HOMA) improved after weight loss with no further improvement during weight maintenance. Cyclin-dependent kinase inhibitor 2B (CDKN2B) and JAZF zinc finger 1 (JAZF1), associated with type 2 diabetes, were downregulated. We could also confirm the downregulation of candidates for obesity and related traits, such as tenomodulin (TNMD) and matrix metallopeptidase 9 (MMP9), with weight loss. The expression of other candidates, such as cell death-inducing DFFA-like effector A (CIDEA) and stearoyl-CoA desaturase (SCD) were upregulated during weight loss but returned to baseline levels during weight maintenance. Conclusion. Genes in the adipose tissue are differentially expressed during weight loss and weight maintenance after weight loss. Genes that show sustained regulation may be of potential interest as markers of the beneficial effects of weight loss whereas others seem to be primarily involved in the process of weight loss itself.
Differential gene expression in adipose tissue from obese human subjects during weight loss and weight maintenance.
Sex, Age
View SamplesDiurnal temperature cycling is an intrinsic characteristic of many exposed microbial ecosystems. However, its influence on yeast physiology and transcriptome has not been studied in detail. In this study, 24-h sinoidal temperature cycles, oscillating between 12 and 30C, were imposed on anaerobic, glucose-limited chemostat cultures of Saccharomyces cerevisiae. After three diurnal temperature cycles (DTC), concentrations of glucose, and extracellular metabolites, as well as CO2-production rates showed regular, reproducible circadian rhytms. DTC also led to waves of transcriptional activation and repression, which involved one sixth of the yeast genome. A substantial fraction of these DTC-responsive genes appeared to primarily respond to changes in glucose concentration. Elimination of known glucose-responsive genes revealed overrepresentation of previously identified temperature-responsive genes as well as genes involved in cell cycle and de novo purine biosynthesis. Analyses of budding index and flow cytomery demonstrated that DTC led to a partial synchronization of the cell cycle of the yeast populations in the chemostat cultures, which was lost upon release from DTC. Comparison of DTC results with data from steady-state cultures showed that DTC was sufficiently slow to allow S. cerevisiae chemostat cultures to almost completely acclimatize their transcriptome and physiology at the DTC temperature maximum, and to approach acclimation at the DTC temperature minimum.
Physiological and transcriptional responses of anaerobic chemostat cultures of Saccharomyces cerevisiae subjected to diurnal temperature cycles.
No sample metadata fields
View SamplesIn order to establish a list of candidate direct COUP-TFI gene targets in the inner ear, we analyzed the differential gene expression profiles of the wild-type and the COUP-TFI/ P0 inner ears.
Genome-wide analysis of binding sites and direct target genes of the orphan nuclear receptor NR2F1/COUP-TFI.
Specimen part
View SamplesGray leaf spot (GLS) disease of maize can be caused by either of two sibling fungal species Cercospora zeina or Cercospora zeae-maydis. These species differ in geographical distribution, for example to date only C. zeina is associated with GLS in African countries, such as South Africa. Maize inbred line B73, which is susceptible to GLS, was planted in the field, and subjected to natural infection with C. zeina. Samples were collected from lower leaves with substantial GLS lesions and younger upper leaves of the same plants with very few immature GLS lesions. The first aim of the experiment was to determine which maize genes are induced in response to C. zeina infection. The second aim was to identify C. zeina genes expressed in planta during a compatible interaction. The third aim was to determine whether the C. zeina cercosporin biosynthetic (CTB) genes are expressed in planta. C. zeina fails to produce cercosporin in vitro in contrast to C. zeae-maydis. Cercosporin is a phytotoxin that is thought to play a role in pathogenicity of several Cercospora spp., however its role in the pathogenicity strategy of C. zeina is currently under investigation. Overall design: To collect material that reflected a difference between C. zeina infected B73 leaves and control B73 leaf material, samples were collected from two lower GLS infected leaves (second and third leaf internode below ear), and two upper leaves with minimal GLS symptoms (second and third internode above ear), respectively. The two lower leaves from each plant were pooled prior to RNA extraction, and the two upper leaves from each plant were pooled prior to RNA extraction. Upper and lower leaf samples from three maize B73 plants were subjected to RNA sequencing individually. The three maize plants were selected randomly as one plant per row from three rows of ten B73 plants each.
Complementation of CTB7 in the Maize Pathogen Cercospora zeina Overcomes the Lack of In Vitro Cercosporin Production.
Specimen part, Subject
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