We analysed the transcriptome of dry seeds (the end product of seed maturation) of three genotypes with different DOG1 expression levels. These included the WT Ler (low DOG1 expression), the near isogenic line NILDOG1-Cvi (strong DOG1 expression) and the non-dormant dog1-1 mutant (absence of DOG1 expression). NILDOG1-Cvi is the Ler WT containing an introgression of the Cvi accession on chromosome 5, which includes the DOG1 gene (Bentsink et al., 2006). The dog1-1 mutant is in the NILDOG1-Cvi genetic background.
The Arabidopsis DELAY OF GERMINATION 1 gene affects ABSCISIC ACID INSENSITIVE 5 (ABI5) expression and genetically interacts with ABI3 during Arabidopsis seed development.
Specimen part
View Samplesaffy_rice_2011_03 - affy_compartimentation_rice_albumen_embryon - During germination, the rice seed goes from a dry quiescent state to an active metabolism. As with all cereals, the rice seed is highly differentiated between the embryo (that will give rise to the future plantlet) and the endosperm (that contains the seed storage compounds and that will degenerate). The molecular mechanisms operating in the rice seed embryo have begun to be described. Yet, very few studies have focused specifically on the endosperm during the germination process. In particular, the endosperm is mostly addressed with regards to its storage proteins but we have detected a large protein diversity by two-dimensional electrophoresis. Similarly, the endosperm is rich in total RNA which suggest that gene expression coming from seed maturation could play a role during the germination process. In this context, we want to compare the transcriptome of the embryo and the endosperm during rice seed germination. -We germinate rice seeds of the first sequenced rice cultivar i.e. Nipponbare during 0, 4, 8, 12, 16 and 24h of imbibition in sterile distilled water. Germination occurs under constant air bubbling, in the dark at 30C. These rice seeds are then manually dissected into embryo and endosperm fractions. -The embryo-derived samples are abbreviated in E while the endosperm samples are abbreviated A. The germination time-point is indicated after the letter (e.g. E8 for embryo samples harvested after 8 hours of germination). Finally, the biological repetition number is indicated before the letter and the time digit (e.g. 1-E8 for an embryo sample from the first repetition at 8 hours of imbibition).
Compartmentation and dynamics of flavone metabolism in dry and germinated rice seeds.
Specimen part
View SamplesGlioblastoma multiforme (GBM) is the most malignant and most common tumor of the central nervous system characterized by rapid growth and extensive tissue infiltration. GBM results in more years of life lost than any other cancer type. Notch signaling has been implicated in GBM pathogenesis through several modes of action. Inhibition of Notch leads to a reduction of cancer-initiating cells in gliomas and reduces proliferation and migration. Deltex1 (DTX1) is part of an alternative Notch signaling pathway distinct from the canonical MAML1/RBPJ-mediated cascade. In this study, we show that DTX1 activates both the RTK/PI3K/PKB as well as the MAPK/ERK pathway. Moreover, we found the anti-apoptotic factor Mcl-1 to be induced by DTX1. In accordance with this, the clonogenic potential and proliferation rates of glioma cell lines correlated with DTX1 levels. DTX1 knock down mitigated the tumorigenic potential in vivo, and overexpression of DTX1 increased cell migration and invasion of tumor cells accompanied by an elevation of the pro-migratory factors PKB and Snail1. Microarray gene expression analysis identified a DTX1-specific transcriptional program - including microRNA-21 - which is distinct from the canonical Notch signaling. We propose the alternative Notch pathway via DTX1 as oncogenic factor in malignant glioma and found low DTX1 expression levels to correlate with prolonged survival of GBM and early breast cancer patients in open source databases.
Deltex-1 activates mitotic signaling and proliferation and increases the clonogenic and invasive potential of U373 and LN18 glioblastoma cells and correlates with patient survival.
Specimen part, Cell line
View SamplesUsing a novel class of chemically-engineered oligonucleotides, termed "antagomirs", we studied the biological significance of silencing miR-122 in the liver of mice at the mRNA level
Silencing of microRNAs in vivo with 'antagomirs'.
No sample metadata fields
View SamplesThe goal of this study was to investigate DNA methylation and gene expression changes in a zebrafish model of ICF Syndrome which were generated by mutation of ICF-gene zbtb24. Comparison of gene expression changes between wildtype and zbtb24 homozygous mutants revealed upregulation of interferon response genes following zbtb24 deletion. Upregulation of interferon response genes was blocked by mutation of the dsRNA helicase Mda5. Overall design: For RNA-seq, gene expression was compared in whole two-week-old zebrafish larvae that were wildtype or homozygous for the zbtb24mk22 mutant allele. We further performed RNA-Seq analysis in three-week-old zebrafish larvae that were WT, mda5mk29/mk29 , zbtb24mk22/mk22 and mda5mk29/mk29 ;zbtb24mk22/mk22. Three samples consisting of pools of 10 larvae were examined for each genotype. For ERRBS, DNA was separately isolated from the fins of three wildtype and three zbtb24mk22 homozygous mutant adults.
Pericentromeric hypomethylation elicits an interferon response in an animal model of ICF syndrome.
Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
TPL-2-ERK1/2 signaling promotes host resistance against intracellular bacterial infection by negative regulation of type I IFN production.
Specimen part
View SamplesAnalysis of Mtb infected murine macrophages derived from C57Bl/6 WT, TPL2KO, IFNARKO & TPL2IFNAR DKO mice [Set 2]
TPL-2-ERK1/2 signaling promotes host resistance against intracellular bacterial infection by negative regulation of type I IFN production.
Specimen part
View SamplesAnalysis of Mtb infected murine macrophages derived from C57Bl/6 WT, TPL2KO, IFNARKO & TPL2IFNAR DKO mice [Set 1]
TPL-2-ERK1/2 signaling promotes host resistance against intracellular bacterial infection by negative regulation of type I IFN production.
Specimen part
View SamplesNatural killer (NK) cells are lymphocytes that participate in immune responses through their cytotoxic activity and secretion of cytokines and chemokines. They can be activated by interaction with ligands on target cells or by soluble mediators such as cytokines. In addition, soluble HLA-G, a major histocompatibility complex molecule secreted by fetal trophoblast cells during early pregnancy, stimulates resting NK cells to secrete proinflammatory and proangiogenic factors. Human NK cells are abundant in uterus, where they remain after implantation. Soluble HLA-G is endocytosed into early endosomes of NK cells where its receptor, CD158d, initiates a signaling cascade through DNA-PKcs, Akt and NF-kB3. The physiological relevance of this endosomal signaling pathway, and how the fate and function of NK cells during early pregnancy is regulated, is unknown. Here we show that soluble agonists of CD158d trigger DNA damage response signaling and p21 (CIP1/WAF1) expression to promote senescence in primary NK cells. CD158d engagement resulted in morphological alterations in cell size and shape, chromatin remodeling, and survival in the absence of proliferation, all hallmarks of senescence. Microarray analysis revealed a senescence signature of upregulated genes upon sustained activation through CD158d. The proinflammatory and proangiogenic factors secreted by these metabolically active NK cells are part of a senescence associated secretory phenotype (SASP) that promoted tissue remodeling and angiogenesis as assessed by functional readouts of vascular permeability and endothelial cell tube formation. We propose that ligand-induced senescence is a molecular switch for the sustained activation of NK cells in response to soluble HLA-G for the purpose of remodeling the maternal vasculature in early pregnancy.
Cellular senescence induced by CD158d reprograms natural killer cells to promote vascular remodeling.
Specimen part, Treatment, Time
View SamplesDespite even large phenotypic differences among vertebrate groups, dentitions and jaws fit and function together, yet the genetic processes that orchestrate cranial and dental morphogenesis remain poorly understood. In the p63-/- mouse mutant, teeth but not jaws fail to form. This edentate mouse is a model with which to tease out genes important for odontogenesis but not jaw morphogenesis, and which may thus allow dentitions to change during development and evolution without necessarily affecting the jaw skeleton. With the working hypothesis that tooth and jaw development are autonomously controlled by discreet gene regulatory networks, we probed for genes crucial for tooth development only. Using gene expression microarray assays validated by quantitative reverse-transcription PCR, we contrasted expression in mandibular prominences at embryonic days (E) 10-13 among mice with normal lower jaw development and either normal (p63+/-, p63+/+) or arrested (p63-/-) tooth development. We predicted that expression of a suite of genes specific to odontogenesis would differ in the edentate mice. The p63-/- mice showed significantly different expression (fold change 1.5, -1.5; p0.05) of several genes, some of which are already reported to help regulate odontogenesis (e.g., p63, Osr2, Cldn3/4) and/or to be targets of p63 (e.g., Jag1/2, Fgfr2), others of which have no previously reported roles in odontogenesis or the p63 pathway (e.g, Fermt1, Cbln1, Pltp, Cxcl14, Krt8, and additional keratin and claudin family members). As expected, from E10-E13 few genes known to regulate mandible morphogenesis differed in expression between mouse strains. Thus this study links for the first time several genes to odontogenesis and/or the p63 signaling network. We propose that these genes act in a novel odontogenic network that is exclusive of lower jaw morphogenesis, and posit that this network evolved in oral, not pharyngeal, teeth.
Detangling the evolutionary developmental integration of dentate jaws: evidence that a p63 gene network regulates odontogenesis exclusive of mandible morphogenesis.
Specimen part
View Samples