Grapevine rootstock 1616C shoots were sterilized and cultured on Murashige & Skoog (MS) medium containing 2% sucrose (w/v). Plantlets were grown in a growth chamber with a 16-h light/8-h dark cycle for 10 weeks at 25 °C.
Salt stress induces endoplasmic reticulum stress-responsive genes in a grapevine rootstock.
Specimen part, Time
View SamplesPotted Cabernet Sauvignon vines in the greenhouse were exposed to irrigated controls, non-irrigated water-deficits, and saline treatments for 16 days. Plant shoot tips were harvested every 4 days (0,4,8,12, and 16 days) to measure the progression of changes of global gene expression due to the stress.
Water and salinity stress in grapevines: early and late changes in transcript and metabolite profiles.
Specimen part
View SamplesEffects of treatment with Nimodipine on N9 cells
Nimodipine fosters remyelination in a mouse model of multiple sclerosis and induces microglia-specific apoptosis.
Treatment
View SamplesHere we show that the histone methyltransferase MLL4 (Kmt2d) is required for stem cell activity and an aggressive form of acute myeloid leukemia (AML) harboring the MLL-AF9 oncogene. MLL4 exerts its function by regulating transcriptional programs associated with the anti-oxidant response. Overall design: The role of Mll4 (Kmt2d) in regulating the transcriptome of primary and transformed hematopoietic stem cells was studied.
DNA-damage-induced differentiation of leukaemic cells as an anti-cancer barrier.
No sample metadata fields
View SamplesBesides symptoms caused by central nervous system (CNS) lesions, the majority of patients with multiple sclerosis (MS) also exhibit gastrointestinal dysfunction that has frequently been noted, but was not directly linked to the autoimmune etiology of the disease.We studied the enteric nervous system (ENS) in a murine model of MS by histology and electron microscopy. Serum IgG against enteric neurons and enteroglia was measured by ELISA and binding to the ENS was confirmed by immunohistochemistry. Target antigens were identified by mass spectrometry. Gastrointestinal dysfunction was determined by measuring dye transit time. RNA expression profiling was conducted with small intestines of MP4-immunized and control-immunized mice. Data from the mouse model were confirmed in MS patients by immunohistochemistry of the ENS in bowel resectates. In addition, ELISA was performed on plasma samples to detect antibodies against four specific target antigens as identified in the mouse model. ENS degeneration was evident already before the onset of clinical disease in the mouse model. Pathology was predominantly antibody-mediated and caused a significant decrease in gastrointestinal transit, which was associated with severe gliosis of the ENS. Unlike the dense infiltrates that developed in the perivascular compartments of the CNS of MP4-immunized mice, the infiltrates in the ENS consisted of single cells scattered throughout the tissue. RNA expression profiling could support these results, as the expression of inflammatory markers in the small intestine was similar between MP4-immunized and HEL-immunized mice. We identified four specific target antigens derived from enteric neurons and/or enteroglia. Antibodies against all four target antigens were present in MS patients. MS patients also showed gliosis and signs of ENS degeneration in the small intestine. For the first time, this study establishes a pathomechanistic link between the well-established autoimmune attack on the CNS and the ENS in MS. The presence of ENS pathology prior to CNS degeneration introduces entirely novel ways to explain MS etiology and immunopathogenesis.
The enteric nervous system is a potential autoimmune target in multiple sclerosis.
No sample metadata fields
View SamplesThe conditioned media from Bifidobacterium infantis (BCM) and Lactobacillus acidophilus (LCM) were reported to promote maturation of innate immune response gene expression, which explained the protective effects of probiotics in clinical necrotizing enterocolitis. We used microarray analysis to investigate the expression of genes involved in regulation of BCM and LCM in IL-1 stimulated immature human enterocytes.
Secreted Metabolites of Bifidobacterium infantis and Lactobacillus acidophilus Protect Immature Human Enterocytes from IL-1β-Induced Inflammation: A Transcription Profiling Analysis.
Specimen part, Cell line
View SamplesIL-10 is a prototypical anti-inflammatory cytokine, which is fundamental to the maintenance of immune homeostasis, especially in the intestine. There is an assumption that cells producing IL-10 have an immunoregulatory function. However, here we report that IL-10-producing CD4+ T cells are phenotypically and functionally heterogeneous. By combining single cell transcriptome and functional analyses, we identified a subpopulation of IL-10-producing Foxp3Neg CD4+ T cells that displays regulatory activity unlike other IL-10-producing CD4+ T cells, which are unexpectedly pro-inflammatory. The combinatorial expression of co-inhibitory receptors is sufficient to discriminate IL-10-producing CD4+ T cells with regulatory function from others and to identify them across different tissues and disease models in mice and humans. These regulatory IL-10-producing Foxp3Neg CD4+ T cells have a unique transcriptional program, which goes beyond the regulation of IL-10 expression. Finally, we found that patients with Inflammatory Bowel Disease (IBD), demonstrate a deficiency in this specific regulatory T-cell subpopulation. Overall design: We carried out high troughput RNA sequencing of RNA isolated from IL-10 producing Foxp3- CD4+ T-cells, which were isolated from the spleen of mice treated with anti-CD3 antibody.
Molecular and functional heterogeneity of IL-10-producing CD4<sup>+</sup> T cells.
Subject
View SamplesGoals of the study:
Global gene expression changes in rat retinal ganglion cells in experimental glaucoma.
No sample metadata fields
View SamplesChromatin in eukaryotic nuclei is organized at multiple scales, from individual nucleosomes to specific loops between regulatory sequences, to the folding of large genomic regions into topological domains and segregation of whole chromosomes into territories. Many of the chromatin proteins that regulate this architecture, including the essential Polycomb Group (PcG) proteins, are themselves organized into subnuclear structures. Deciphering mechanistic links between protein organization and genome architecture requires precise description and mechanistic perturbations of both. Using super-resolution microscopy, we characterized the nanoscale organization of PcG proteins in Drosophila cells and find hundreds of small protein clusters, distinct from the large PcG bodies present in just a few copies per cell that have been the focus of previous investigations. We manipulated PcG clusters either by disrupting the polymerization activity of the conserved Sterile Alpha Motif (SAM) of the PcG protein Polyhomeotic (Ph) or increasing Ph levels in Drosophila S2 cells. Disrupting clustering using Ph SAM mutations disrupts chromatin interactions on scales from 50kb to 13Mb while increasing Ph levels increases both cluster number and long range chromatin interactions. RNA-seq and qPCR indicate that both perturbations also alter expression levels of many genes. Molecular simulations suggest a model in which PcG cluster formation on chromatin is governed by the kinetics of association between Ph SAMs and PcG cluster size is bounded by the affinity and occupancy of chromatin binding sites. Our results suggest that nanoscale organization of PcG proteins into small, abundant clusters on chromatin through the polymerization activity of Ph SAM shapes genome architecture by mediating numerous long-range chromatin interactions. Overall design: Two biological replicates of three RNA-seq samples from S2 cells, cells overexpresing wild-type Ph, and cells overexpressing polymerization defective Ph-ML
Chromatin topology is coupled to Polycomb group protein subnuclear organization.
Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A multiply redundant genetic switch 'locks in' the transcriptional signature of regulatory T cells.
Sex, Age, Specimen part
View Samples