Purpose: Breeding for gibberella ear rot resistance have been challenging due to the high complexity of the trait. The current study attempts to characterize defence responses to Fusarium graminearum infection in two maize inbred lines with different levels of resistance to the pathogen. Methods: RNA was extracted from developing kernels of two inbred lines, which had been either fungal (F. graminearum DAOM180378) or mock inoculated 11 days post sibcrossing, using a guanidine isothiocyanate method and ultra-centrifugation with cesium chloride. Isolated RNA was used to quantify whole genome gene expression using RNA-seq (Illumina TruSeq RNA library prep kit v2, Illumina HiSeq 2000). Paired end reads generated from RNA-seq were trimmed of adaptors and low quality reads, aligned with the B73 reference genome sequence version 2, expression levels (TPM) were computed and differential gene expression analysis were performed using CLC Genomics Workbench version 9. Results: Gene transcripts responding to fungal infection were captured by comparing gene expression levels in mock and fungal inoculated maize ears and gene ontology terms associated with significantly up-regulated gene transcripts were determined for each inbred. More genes were up regulated in the susceptible inbred relative to the resistant inbred, many of which are associated with oxidation-reduction processes potentially causing earlier programmed cell death in the susceptible inbred. Conclusions: This information helped to identify gene transcripts that were relevant in defense responses with potential applicability in routine breeding efforts and to propose an effective GER resistance mechanism. Overall design: The experiment consisted of 16 RNA samples from two inbreds (B73 and CO441) tested over two years (2004 and 2006), two treatments (mock and fungal) and two sampling times (1 and 2 days after inoculation).
Transcriptome profiling of two maize inbreds with distinct responses to Gibberella ear rot disease to identify candidate resistance genes.
Specimen part, Treatment, Subject
View SamplesWe report application of RNA-seq to quantify gene expression changes in fasted mouse livers compared to re-fed controls. Overall design: RNA-seq from livers of re-fed and 48h fasted mice.
Histone propionylation is a mark of active chromatin.
Sex, Specimen part, Treatment, Subject
View SamplesIsoform quantification results for B6 mouse using Bowtie and RSEM. Overall design: ~400 islets were isolated and pooled from two B6 mice. Whole islet RNA was isolated using Rneasy purification columns (Qiagen), quantified (Nanodrop) and integrity verified (Agilent) prior to sequencing. ~94M total paired-end RNA-Seq reads were sequenced.
The Transcription Factor Nfatc2 Regulates β-Cell Proliferation and Genes Associated with Type 2 Diabetes in Mouse and Human Islets.
Specimen part, Cell line, Subject
View SamplesMeg3 is a long non-coding RNA. It's target genes are unknown. The mouse pancreatic beta cell line MIN6-4N was used to assess the expression of genes upon stable Meg3 overexpression
Epigenetic regulation of the lncRNA MEG3 and its target c-MET in pancreatic neuroendocrine tumors.
Specimen part, Cell line
View SamplesElevated branched chain amino acids (BCAAs) are associated with obesity and insulin resistance. How long-term dietary BCAAs impact late-life health and lifespan is unknown. Here, we show that when dietary BCAAs are varied against a fixed, isocaloric macronutrient background, long-term exposure to high BCAA diets led to hyperphagia, obesity and reduced lifespan. These effects were not due to elevated BCAA per se or hepatic mTOR activation, but rather the shift in balance between dietary BCAAs and other AAs, notably tryptophan and threonine. Increasing the ratio of BCAAs to these AAs resulted in hyperphagia and was linked to central serotonin depletion. Preventing hyperphagia by calorie restriction or pair-feeding averted the health costs of a high BCAA diet. Our data highlight a role for amino acid quality in energy balance and show that health costs of chronic high BCAA intakes were not due to intrinsic toxicity; rather, to hyperphagia driven by AA imbalance. Overall design: 3 animals per sex per diet were used. Mice were fed one of four diets (all 19% total protein, 63% carbohydrate, 18% fat, total energy density 14 kJ/g) varying in BCAA content (BCAA200: twice BCAA content of control diet AIN93G; BCAA100: standard content of BCAAs; and BCAA50 and BCAA20: containing one half and one fifth of standard content of BCAAs), and either euthanized at 15 months of age or maintained for determination of lifespan.
Branched chain amino acids impact health and lifespan indirectly via amino acid balance and appetite control.
Sex, Age, Specimen part, Cell line, Subject
View SamplesCholesterol is one of the key molecules in mammals and the most striking examples of its deficiency are the inborn errors of cholesterol biosynthesis that manifest in severe whole body phenotypes. Liver, the principal site of cholesterol homeostasis, has rarely been investigated in these defects. We thus focused on the hepatocyte-specific deletion of lanosterol 14-demethylase (CYP51) catalyzing the rate-limiting step in the post-squalene part of cholesterol synthesis.
Lessons from hepatocyte-specific Cyp51 knockout mice: impaired cholesterol synthesis leads to oval cell-driven liver injury.
Sex, Specimen part, Treatment
View SamplesWe investigated the association between subgingival bacterial profiles and gene expression patterns in gingival tissues of patients with periodontitis.
Subgingival bacterial colonization profiles correlate with gingival tissue gene expression.
Specimen part
View SamplesWe examined gene expression signatures in healthy and diseased gingival tissues in 90 patients. Analysis of the gingival tissue transcriptome in states of periodontal health and disease may reveal novel insights of the pathobiology of periodontitis.
Transcriptomes in healthy and diseased gingival tissues.
Specimen part
View SamplesBackground: Venous hypertension is often present in advanced and in acute decompensated heart failure (HF). However, it is unclear whether high intravenous pressure can cause alterations in homeostasis by promoting inflammation and endothelial cell (EC) activation. We used an experimental model of acute, local venous hypertension to study the changes in circulating inflammatory mediators and EC phenotype that occur in response to biomechanical stress. Methods and Results: Twenty-four healthy subjects (14 men, age 352 years) were studied. Venous arm pressure was increased to ~30 mmHg above baseline level by inflating a tourniquet cuff around the dominant arm (test arm). Blood and endothelial cells (ECs) were sampled from test and control arm (lacking an inflated cuff) before and after 75 minutes of venous hypertension, using angiocatheters and endovascular wires. Magnetic beads coated with EC specific antibodies were used for EC separation; amplified mRNA was analyzed by Affymetrix HG-U133 2.0 Microarray. Plasma endothelin-1 (ET-1), interleukin-6 (IL-6), vascular cell adhesion molecule-1 (VCAM-1) and chemokine (C-X-C motif) ligand 2 (CXCL2) were significantly increased in the congested arm. 5,332 probe sets were differentially expressed in venous ECs before vs. after testing. Among the 143 probe sets that exhibited a significant absolute fold change >2, we identified several inflammatory mediators including ET-1, VCAM-1, and CXCL2. Conclusions: Acute experimental venous hypertension is sufficient to cause local increase in circulating inflammatory mediators and to activate venous ECs in healthy human subjects. Additional work is needed to determine the effect of venous hypertension in patients with established HF.
Peripheral venous congestion causes inflammation, neurohormonal, and endothelial cell activation.
Specimen part, Treatment, Subject
View SamplesBalanced immune responses in airways of patients with asthma are crucial to succesful clearance of viral infection and proper asthma control.
Rhinovirus-induced epithelial RIG-I inflammasome suppresses antiviral immunity and promotes inflammation in asthma and COVID-19.
Subject, Time
View Samples