This study aimed to generate a comprehensive analysis of changes in the transcriptome following MNV infection. Furthermore, we aimed to perform a differential gene expression analysis between MNV infection and loxoribine (tlr7 agonist) treatment to delineate features of the host modified directly by the MNV as opposed to indirect changes induced through IFN signalling. Overall design: Transcript expression profiles of RAW264.7 cells mock infected, infected with MNV (MOI 5) or treated with loxoribine (1 mM) for 12 hrs were generated using Illumina NextSeq500.
RNA Sequencing of Murine Norovirus-Infected Cells Reveals Transcriptional Alteration of Genes Important to Viral Recognition and Antigen Presentation.
Cell line, Subject
View SamplesThe transcriptome has an abundance of information about the function of individual cells, tissues and an organism in general. Characterising the transcriptome of virus infected cells can illuminate features of the viral-host relationship that are important for pathogenesis. This study broadly aimed to quantify the host gene expression changes that occur following MNV infection. Furthermore, we aimed to identify alterations in specific biological pathways by identifying alterations in transcript abundance that increase or decrease in intensity with MNV infection over time. Overall design: Transcript expression profiles of RAW264.7 cells mock infected or infected with MNV for 4, 8, 12, 16 and 20 hours (MOI 5) were generated by RNA-sequencing using Illumina NextSeq500.
RNA Sequencing of Murine Norovirus-Infected Cells Reveals Transcriptional Alteration of Genes Important to Viral Recognition and Antigen Presentation.
Cell line, Subject, Time
View SamplesRNA sequencing data of macrophages after differentiation in the presence of TPC1 thyroid cancer cell line Overall design: Co-incubation in trans-well system between TPC1 cell lines and human primary macrophages
Transcriptional and metabolic reprogramming induce an inflammatory phenotype in non-medullary thyroid carcinoma-induced macrophages.
No sample metadata fields
View SamplesA large-scale parallel expression analysis was conducted to elucidate Mla-specified responses to powdery mildew infection using 22K Barley1 GeneChip probe arrays. Our goal was to identify genes differentially expressed in incompatible (resistant) vs. compatible (susceptible) and Mla-specified Rar1-dependent vs. -independent interactions. A split-split-plot design with 108 experimental units (3 replications x 2 isolates x 3 genotypes x 6 time points) was used to profile near-isogenic lines containing the Mla1, Mla6, and Mla13 resistance specificities in response to inoculation with the Blumeria graminis f. sp. hordei (Bgh) isolates 5874 (AvrMla1, AvrMla6) and K1 (AvrMla1, AvrMla13). ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Rico Caldo. The equivalent experiment is BB4 at PLEXdb.]
Interaction-dependent gene expression in Mla-specified response to barley powdery mildew.
Specimen part, Time
View SamplesTime-course expression profiles of Bgh challenged barley cultivar C.I. 16151 (harboring the Mla6 powdery mildew resistance allele) and its fast-neutron-derived "Bgh-induced tip cell death1" mutant, bcd1, were compared using the 22K Barley1 GeneChip. Planting, stage of seedlings, harvesting, and experimental design were part of a larger experiment described by Caldo et al. (2004). PLEXdb BB4. Experiment Design: C.I. 16151 (wildtype) and bcd1 (mutant) were planted in separate 20 x 30-cm flats using sterilized potting soil. Each experimental flat consisted of six rows of 15 seedlings, with rows randomly assigned to one of six harvest time points (0, 8, 16, 20, 24, and 32 hai). Seedlings grown to the 1st leaf stage with 2nd leaf unfolded were inoculated with a high density of fresh conidiospores (84 +/- 19 spores/mm2). Groups of flats were placed at 18C (8-hour darkness, 16-hour light) in separate controlled growth chambers corresponding to the Bgh isolates. Rows of plants were harvested at each assigned time points and snap frozen in liquid nitrogen. The entire experiment was repeated three times in a standard split-split-plot design with 72 experimental units (2 genotypes x 2 pathogen isolates x 6 time points x 3 replications). Treatment Description: The samples constituted pairwise combinations of the the cultivar C.I. 16151(containing the Mla6 resistance allele), and its fast-neutron-derived "Bgh-induced tip cell death1" mutant, bcd1 with the two Bgh (Blumeria graminis f. sp. hordei) isolates, 5874 (AvrMla6, AvrMla1) and K1 (AvrMla13, AvrMla1). For each replication, individual genotypes were planted in separate 20 x 30 cm flats using sterilized potting soil. Each experimental flat consisted of six rows of 15 seedlings, with rows randomly assigned to one of six harvest times (0, 8, 16, 20, 24, and 32 hai). Seedlings were grown to the 2nd-leaf stage with 1st leaf unfolded, and inoculation was performed at 4 PM Central Standard Time by tipping the flats at 45oC and dusting the plants with a high density of fresh conidiospores [84 +/- 19 spores/mm2]. This procedure was repeated from the opposite angle to ensure that a high proportion of the cells are in contact with the fungus. This conidial density per unit leaf area routinely results in greater than 50% of epidermal cells that are successfully infected. Groups of flats were placed at 18oC (8 hours darkness, 16 hours light, 8 hours darkness) in separate controlled growth chambers corresponding to the Bgh isolate. Rows of plants were harvested at their assigned harvest times and flash-frozen in liquid nitrogen. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Roger P Wise. The equivalent experiment is BB46 at PLEXdb.]
Interaction-dependent gene expression in Mla-specified response to barley powdery mildew.
Age, Specimen part, Time
View SamplesA large-scale parallel expression analysis was conducted to elucidate Mla-specified responses to powdery mildew infection using 22K Barley1 GeneChip probe arrays. Our goal was to identify genes differentially expressed in incompatible (resistant) vs. compatible (susceptible) and Mla-specified Rar1-dependent vs. -independent interactions. A split-split-plot design with 108 experimental units (3 replications x 2 isolates x 3 genotypes x 6 time points) was used to profile near-isogenic lines containing the Mla1, Mla6, and Mla13 resistance specificities in response to inoculation with the Blumeria graminis f. sp. hordei (Bgh) isolates 5874 (AvrMla1, AvrMla6) and K1 (AvrMla1, AvrMla13).
Interaction-dependent gene expression in Mla-specified response to barley powdery mildew.
Age, Specimen part, Disease, Disease stage, Cell line, Time
View SamplesA large-scale time course expression profiling of wild type (Mla12/Rar1/Rom1) and mutants (mla12-M66, M82 (rar1-1), M100 (rar1-2) and rom1) of barley cultivar Sultan 5 was conducted to understand the molecular mechanisms of delayed powdery mildew resistance. Barley plants were inoculated with powdery mildew pathogen isolate 5874. First leaves of inoculated and non-inoculated plants were harvested at six time points after pathogen inoculation. The experiment was laid out in split-split-plot design with 180 experimental units (3 replications x 2 treatments (inoculated and non-inoculated) x 5 genotypes x 6 time points).
Stage-specific suppression of basal defense discriminates barley plants containing fast- and delayed-acting Mla powdery mildew resistance alleles.
Age, Specimen part, Time
View SamplesHD11 cells were stimulated with 1 ug/ml endotoxin from ST-798 for 1, 2, 4 and 8 hours
Unique genome-wide transcriptome profiles of chicken macrophages exposed to Salmonella-derived endotoxin.
Cell line, Time
View SamplesThe Atss3 mutant and WT plants were arranged according to a Randomized Complete Block Design. The plants were planted in rows with seven rows in each flat; two plants of the same genotype/pot. Plants were grown under a SD photoperiod (8 h light/16 h dark) in a growth chamber as described. Eight randomly selected rows were harvested for each time point from different flats. Plant material was harvested at five time points in the diurnal cycle (1, 4, 8.5, 12, and 16 h; Time 0 is the beginning of the light period); harvesting was conducted under a green safety light. Each sample consisted of rosette leaves (leaves 5 to 8, staged following Bowmann (1994); photosynthetically active (Stessman et al., 2002)) from sixteen six-week-old plants. Leaf samples were frozen in liquid N2 immediately after harvest and stored at -80C for RNA extraction. The experiment was done twice and independent randomizations for plant growth and harvest were used for the two replicates.
Identification of the novel protein QQS as a component of the starch metabolic network in Arabidopsis leaves.
No sample metadata fields
View SamplesRecent studies have identified intracellular metabolism as a fundamental determinant of macrophage function. In obesity, proinflammatory macrophages accumulate in adipose tissue and trigger chronic low-grade inflammation, that promotes the development of systemic insulin resistance, yet changes in their intracellular energy metabolism are currently unknown. We therefore set out to study metabolic signatures of adipose tissue macrophages (ATMs) in lean and obese conditions. F4/80-positive ATMs were isolated from obese vs lean mice. High-fat feeding of wild-type mice and myeloid-specific Hif1-/- mice was used to examine the role of hypoxia-inducible factor-1 (HIF-1) in ATMs part of obese adipose tissue. In vitro, bone marrow-derived macrophages were co-cultured with adipose tissue explants to examine adipose tissue-induced changes in macrophage phenotypes. Transcriptome analysis, real-time flux measurements, ELISA and several other approaches were used to determine the metabolic signatures and inflammatory status of macrophages. In addition, various metabolic routes were inhibited to determine their relevance for cytokine production. Transcriptome analysis and extracellular flux measurements of mouse ATMs revealed unique metabolic rewiring in obesity characterised by both increased glycolysis and oxidative phosphorylation. Similar metabolic activation of CD14+ cells in obese individuals was associated with diabetes outcome. These changes were not observed in peritoneal macrophages from obese vs lean mice and did not resemble metabolic rewiring in M1-primed macrophages. Instead, metabolic activation of macrophages was dose-dependently induced by a set of adipose tissue-derived factors that could not be reduced to leptin or lactate. Using metabolic inhibitors, we identified various metabolic routes, including fatty acid oxidation, glycolysis and glutaminolysis, that contributed to cytokine release by ATMs in lean adipose tissue. Glycolysis appeared to be the main contributor to the proinflammatory trait of macrophages in obese adipose tissue. HIF-1, a key regulator of glycolysis, nonetheless appeared to play no critical role in proinflammatory activation of ATMs during early stages of obesity. Our results reveal unique metabolic activation of ATMs in obesity that promotes inflammatory cytokine release. Further understanding of metabolic programming in ATMs will most likely lead to novel therapeutic targets to curtail inflammatory responses in obesity.
Unique metabolic activation of adipose tissue macrophages in obesity promotes inflammatory responses.
Sex, Specimen part
View Samples