Red light can affect a variety of responses in Arabidopsis. We characterize the early gene expression patterns of seedlings exposed to 1 hour of red light using a small sized sample of 5, 7-day-old seedlings and also performed dark controls.
Extraction and labeling methods for microarrays using small amounts of plant tissue.
No sample metadata fieldsView Samples
This study analyzes transcriptome profiles in pre-germinated seeds and hypoxia-treated seedlings of Arabidopsis thaliana wild type (Col-0) and homozygous mutants (prt6-1 and ate1 ate2). This dataset includes CEL files, RMA signal values and MAS5 P/M/A calls. For pre-germinated seeds, seeds imbibed for 24 h were used for total RNA extraction. For hypoxia treatment, 7-d-old seedlings were incubated in a hypoxia chamber for 2 h and the entire seedling was subjected to RNA extraction. Quantitative profiling of cellular mRNAs was accomplished with the Affymetrix ATH1 platform. Changes in the transcriptome during early seed germination stage and in response to hypoxia in seedlings were evaluated. The data led to identification of mRNAs with abundance regulated by PRT6 and ATE1 / ATE2, which are essential components for the N-end rule pathway of targeted proteolysis (NERP). A combination of genetic, biochemical and molecular analyses reveal that NERP coordinates the stability of key ethylene responsive factor (ERF) family transcription factors, which regulate expression of core hypoxia response genes and tolerance to low oxygen stress. This indicates that the NERP functions as a homeostatic sensor of low oxygen in plants.
Homeostatic response to hypoxia is regulated by the N-end rule pathway in plants.
Age, Specimen part, TreatmentView Samples
These investigations studied the fundamentals of how plants perceive gravity and develop in microgravity. It informs how gene regulation is altered by spaceflight conditions.
Comparative transcriptomics indicate changes in cell wall organization and stress response in seedlings during spaceflight.
Specimen partView Samples
S. epidermidis ability to form biofilms on indwelling medical devices and its association with the emergence of chronic infections is its main virulence factor. Nevertheless, it has been shown that the cells released from these biofilms are associated with the advent of serious acute infections with bacteraemia as one of the major clinical manifestations. Despite their clinical relevance, very little is known about the impact of biofilm-released cells in pathogenesis. Hence, herein, we characterized the murine immune response to the presence of cells released from S. epidermidis biofilms analysing spleen cells transcriptome by microarrays. These findings may help to explain the recurrent inflammatory symptoms presented by patients with colonization of indwelling medical devices.
<i>Staphylococcus epidermidis</i> Biofilm-Released Cells Induce a Prompt and More Marked <i>In vivo</i> Inflammatory-Type Response than Planktonic or Biofilm Cells.
Sex, Specimen partView Samples
The evolutionarily conserved Wnt/?-catenin signaling pathway plays a fundamental role during metazoan development, regulating numerous processes including cell fate specification, cell migration, and stem cell renewal. Wnt ligand binding leads to stabilization of the transcriptional effector ?-catenin and upregulation of target gene expression to mediate a cellular response. During larval development of the nematode Caenorhabditis elegans, Wnt/?-catenin pathways act in fate specification of two hypodermal cell types, the ventral vulval precursor cells (VPCs) and the lateral seam cells. Because little is known about targets of the Wnt signaling pathways acting during larval VPC and seam cell differentiation, we sought to identify genes regulated by Wnt signaling in these two hypodermal cell types. We conditionally activated Wnt signaling in larval animals and performed cell type?specific "mRNA tagging" to enrich for VPC and seam cell?specific mRNAs, and then used microarray analysis to examine gene expression compared to control animals. Two hundred thirty-nine genes activated in response to Wnt signaling were identified, and we characterized 50 genes further. The majority of these genes are expressed in seam and/or vulval lineages during normal development, and reduction of function for nine genes caused defects in the proper division, fate specification, fate execution, or differentiation of seam cells and vulval cells. Therefore, the combination of these techniques was successful at identifying potential cell type?specific Wnt pathway target genes from a small number of cells and at increasing our knowledge of the specification and behavior of these C. elegans larval hypodermal cells.
Identification of Wnt Pathway Target Genes Regulating the Division and Differentiation of Larval Seam Cells and Vulval Precursor Cells in Caenorhabditis elegans.
Specimen partView Samples
Mild vs. severe psoriasis vulgaris is often distinguished by the Psoriasis Area and Severity Index. It is widely assumed that severe psoriasis involves higher levels of skin inflammation, but comparative molecular profiles of mild vs. severe disease have not been previously performed. In this study, we used gene arrays to phenotype North American patients with mild psoriasis vs. severe psoriasis.
The Spectrum of Mild to Severe Psoriasis Vulgaris Is Defined by a Common Activation of IL-17 Pathway Genes, but with Key Differences in Immune Regulatory Genes.
Disease, Disease stageView Samples
We sought to characterize delayed-type hypersensitivity (DTH) responses elicited by topical hapten DPCP in normal human skin
Molecular characterization of human skin response to diphencyprone at peak and resolution phases: therapeutic insights.
Specimen part, Subject, TimeView Samples
Chromatin architectural protein NSBP1/HMGN5 belongs to the family of HMGN proteins which specifically interact with nucleosomes via Nucleosome Binding Domain, unfold chromatin and affect transcription. Mouse NSBP1 is a new and uncharacterized member of HMGN protein family. NSBP1 is a nuclear protein which is localized to euchromatin, binds to linker histone H1 and unfolds chromatin.
The interaction of NSBP1/HMGN5 with nucleosomes in euchromatin counteracts linker histone-mediated chromatin compaction and modulates transcription.
No sample metadata fieldsView Samples
CTLA-4 is thought to inhibit effector T cells both intrinsically, by competing with CD28 for B7 ligands, and extrinsically, through the action of regulatory T cells. We studied in vivo responses of normal and CTLA-4-deficient antigen-specific murine effector CD4+ T cells. In order to do these studies in a physiological model of immunity to foreign antigen, we transferred small numbers of congenically marked RAG2-deficient 5C.C7 T cells with either a normal or knockout allele of CTLA-4 into normal syngeneic B10.A recipient mice. The T cells were then activated by immunization with MCC peptide and LPS. To look for transcriptional signatures of negative regulation of T cell responses by CTLA-4, we used microarray analysis to compare transcripts in wild type and CTLA-4 KO 5C.C7 T cells four days after immunization. This is the first instance in which differences are observed in extent of accumulation of wild type and CTLA-4 KO 5C.C7 T cells.
Cutting edge: CTLA-4 on effector T cells inhibits in trans.
Specimen partView Samples
Cardiac fibroblasts convert to myofibroblasts with injury to mediate healing after acute myocardial infarction and to mediate long-standing fibrosis with chronic disease. Myofibroblasts remain a poorly defined cell-type in terms of their origins and functional effects in vivo. Methods: Here we generate Postn (periostin) gene-targeted mice containing a tamoxifen inducible Cre for cellular lineage tracing analysis. This Postn allele identifies essentially all myofibroblasts within the heart and multiple other tissues. Results: Lineage tracing with 4 additional Cre-expressing mouse lines shows that periostin-expressing myofibroblasts in the heart derive from tissue-resident fibroblasts of the Tcf21 lineage, but not endothelial, immune/myeloid or smooth muscle cells. Deletion of periostin+ myofibroblasts reduces collagen production and scar formation after myocardial infarction. Periostin-traced myofibroblasts also revert back to a less activated state upon injury resolution. Conclusions: Our results define the myofibroblast as a periostin-expressing cell-type necessary for adaptive healing and fibrosis in the heart, which arises from Tcf21+ tissue-resident fibroblasts. Overall design: Fluidigm C1 whole genome transcriptome analysis of lineage mapped cardiac myofibroblasts
Genetic lineage tracing defines myofibroblast origin and function in the injured heart.
Specimen part, Cell line, SubjectView Samples