Fusarium head blight (FHB) is a major disease of cereal crops caused by the fungus Fusarium graminearum (Fg). FHB affects the flowering heads (or spikes) and developing seeds. This study compare the gene expression profile in wheat spikelets (spk 2) inoculated with either water (mock treatment) or a pathogenic strain of Fusarium graminearum (WT); spikelets 2 were inoculated 24 hrs after a neighbour spikelet (spk 0) was treated with either water or F. graminerum mutant strain Tri6 or NoxAB. Spikelets 2 were sampled 8 and 24 hrs after the second treatment.
Components of priming-induced resistance to Fusarium head blight in wheat revealed by two distinct mutants of Fusarium graminearum.
Specimen part
View SamplesThe histone acetyltransferase (HAT) Mof is essential for mouse embryonic stem cells (mESC) pluripotency and early development. Mof is the enzymatic subunit of two different HAT complexes, MSL (Male-Specific Lethal) and NSL (Non-specific lethal). The individual contribution of MSL and NSL complexes to transcription regulation in mESCs is not well understood. Our genome-wide analysis of MSL and NSL localization show that i) MSL and NSL bind to specific and common sets of expressed genes, ii) NSL binds at promoters, iii) while MSL binds in gene bodies. Knockdown of Msl1 leads to a global loss of histone H4K16ac indicating that MSL is the main HAT acetylating H4K16 in mESCs. MSL was enriched at many mESC-specific genes, but also at bivalent domains. Thus, NSL and MSL HAT complexes differentially regulate specific sets of expressed genes in mESCs. Furthermore, MSL is essential for the regulation of key mESC-specific and bivalent developmental genes.
Mof-associated complexes have overlapping and unique roles in regulating pluripotency in embryonic stem cells and during differentiation.
No sample metadata fields
View SamplesBiallelic defects of the gene encoding for the intracellular enzyme 3’ repair exonuclease (Trex)1 cause Aicardi-Goutières syndrome (AGS), a rare monogenic, lupus-like autoimmune disease, while heterozygous Trex1 loss of function alleles are associated with systemic lupus erythematosus (SLE). Trex1-/- mice develop lethal autoimmune multi-organ inflammation, which results from a chronic type I IFN response triggered by intracellular accumulation of a putative nucleic acid substrate of Trex1. This pathogenic nucleic acid is detected by the broadly, but not ubiquitously, expressed cytosolic DNA sensor cGAS, raising the question whether there are specific cell types that respond to Trex1 deficiency by production of IFN and induce autoimmunity. We generated mice with conditional knock out of the Trex1 gene and demonstrated that loss of Trex1 throughout the hematopoietic system and even selective loss in dendritic cells is sufficient to cause IFN release and autoimmunity. B cells showed no transcriptional response to Trex1 deficiency. Trex1-/- keratinocytes produced IFN but did not induce skin inflammation, whereas loss of Trex1 in cardiomyocytes triggered neither IFN response nor pathology. Trex1-deficient neurons and astrocytes did not release IFN in the CNS. In contrast, mice with selective inactivation of Trex1 in long-living CNS macrophages such as microglia locally produced IFN but did not reproduce the mild encephalitis seen in Trex1-/- mice. Collectively, individual cell types differentially respond to the loss of Trex1 and dendritic cells seem promising candidates for experiments addressing the molecular pathomechanism in Trex1 deficiency. Overall design: We sorted CD19-positive B cells from spleens of Trex1fl/fl CD19-Cre+ and Trex1fl/fl CD19-Cre- mice and isolated total RNA for library construction to perform mRNA deep sequencing.
Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic Autoimmunity.
Specimen part, Subject
View SamplesIL17-producing ?d T cells (?d T17) mainly develop in the prenatal phase and persist as long-living self-renewing effector cell in all kind of tissues. They express polyclonal T-cell receptors (TCR), comprising public V?4+ and V?6+ TCRs with germline-like rearrangements. In particular, V?6+ T cells have recently been found in a variety of tissues including enthesis, gingiva or skin. However, their exchange between tissues and the mechanisms of tissue-specific adaptation and residency remain poorly understood. Here, we profiled V?6+ T cells isolated from thymus, peripheral lymph nodes (pLN) and skin through single-cell RNA-seq technology and compared those to V?4+ T cells. Our data demonstrated that V?6+ T cells formed highly homogenous cell populations that could be separated by tissue-specific gene expression signatures. Overall design: Sort V?4 and V?6 ?dT cells from peripheral lymph nodes, ear skin and thymus, then do 3'-RNA single cell sequencing (10x genomics).
Single-Cell Transcriptomics Identifies the Adaptation of Scart1<sup>+</sup> Vγ6<sup>+</sup> T Cells to Skin Residency as Activated Effector Cells.
Age, Specimen part, Cell line, Subject
View SamplesSkeletal muscle actin mice (Crawford et al., (2002) Mol Cell Biol 22, 5587) were crossed with cardiac actin transgenic mice (termed "ACTC^Coco" or "Coco" for short), to produce mice that had cardiac actin instead of skeletal muscle actin in their skeletal muscles (termed "ACTC^Co/KO" or for short "Coco/KO"). Microarray analysis using the Illumina mouse-6 v1.1 expression beadchip was performed on RNA extraced from the soleus muscle of Coco/KO mice and wildtype mice, to confirm the swith in actin isoform expression, and to determine what other differences might exist between wildtype mice and the Coco/KO mice.
Rescue of skeletal muscle alpha-actin-null mice by cardiac (fetal) alpha-actin.
No sample metadata fields
View SamplesThe goal was to screen for the expressed genes in Semi-Circular Canal Duct (SCCD) that are related to ion transport and its regulation. The objectives was to discover which genes changed expression levels in response to glucocorticoids.
Ion transport regulation by P2Y receptors, protein kinase C and phosphatidylinositol 3-kinase within the semicircular canal duct epithelium.
Specimen part
View SamplesThe goal was to screen for the expressed genes in Reissner's membrane (RM) that are related to ion transport and its regulation. The objectives were 1) to determine whether short-term incubation altered the transcriptome and 2 ) to discover which genes changed expression levels in response to glucocorticoids.
Regulation of ENaC-mediated sodium transport by glucocorticoids in Reissner's membrane epithelium.
Specimen part
View SamplesNon-steroidal anti-inflammatory drugs (NSAIDs) are used extensively as therapeutic agents, despite their well-documented gastrointestinal (GI) toxicity. Presently, the mechanisms responsible for NSAID-associated GI damage are incompletely understood. In this study, we used Microarray analysis to generate a novel hypothesis about cellular mechanisms that underlie the GI toxicity of NSAIDs. Monolayers of intestinal epithelial
Drug-induced alterations to gene and protein expression in intestinal epithelial cell 6 cells suggest a role for calpains in the gastrointestinal toxicity of nonsteroidal anti-inflammatory agents.
Specimen part
View SamplesDespite the availability of large-scale transcriptomics data, specific long noncoding RNAs (lncRNAs) expressed in specific brain regions and populations of neurons are poorly understood. Here we report analysis of expression of lncRNAs and mRNAs expressed in hippocampus and prefrontal cortex (PFC), two regions of brain that are involved in memory storage and neuropsychiatric disorders. Our unbiased analyses have identified specific lncRNAs and mRNAs that are enriched in hippocampus and PFC. We have identified several regions in the chromosomes characterized by clustered lncRNA expression suggesting the transcriptional hotspots of lncRNA in the genome. We find that, a subset of lncRNAs and protein coding genes in their vicinity are uniquely co-expressed in specific brain regions and thus presumably co-regulated. Furthermore, specific brain regions and neuronal populations have characteristic lncRNA expression profile. These studies reveal unexpected complexity in the expression profiles of lncRNAs in the mammalian brain. Overall design: Examination of mRNAs and long noncoding RNAs in mouse hippocampus and prefrontal cortex of 8 adult mice.
Transcriptome analyses of adult mouse brain reveal enrichment of lncRNAs in specific brain regions and neuronal populations.
No sample metadata fields
View SamplesTGF-beta has an oncogenic response in glioblastoma and it is considered to be a therapeutic target. We evaluated the effect of TGF-beta inhibition in glioblastoma.
TGF-β Receptor Inhibitors Target the CD44(high)/Id1(high) Glioma-Initiating Cell Population in Human Glioblastoma.
Specimen part, Treatment
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