Boron is an essential micronutrient for plants and is taken up in the form of boric acid (BA). Despite this, a high BA concentration is toxic for the plants, inhibiting root growth and is thus a significant problem in semi-arid areas in the world. In this work, we report the molecular basis for the inhibition of root growth caused by boron. We used microarrays to detail the global gene expression underlying boron toxicity in roots.
A molecular framework for the inhibition of Arabidopsis root growth in response to boron toxicity.
Specimen part, Treatment
View Samplesdifferential expression between wild-type pistils of Arabidopsis thaliana at late 11 to late 12 floral stages, and similar stage pistils of coatlique mutant which lacks a functional embryo sac
Genetic subtraction profiling identifies genes essential for Arabidopsis reproduction and reveals interaction between the female gametophyte and the maternal sporophyte.
Specimen part
View SamplesThe project aims to identify differentially expressed genes in adipose progenitors that were freshly isolated from wild-type or Nr4a1-/- mice. The AP preparation involved adipose tissue digestion, and negative selection of the stromal vascular fraction (depletion of CD31+ endothelial cells and Lineage positive cells. Overall design: 16 samples were anlyzed. 4 groups of adipose progenitors were isolated from subcutaneou(SAT) and visceral (VAT) adipose tissue from Nr4a1 wildtype(Nr4a1+/+) and knockout(Nr4a1-/-) mice. Each group has 4 biological replicates.
Targeting nuclear receptor NR4A1-dependent adipocyte progenitor quiescence promotes metabolic adaptation to obesity.
Subject
View SamplesTo identify of candidate transcriptional regulators of AP function, microarray was utilized to analyze gene expression in freshly isolated AP from stromal-vascular fractions relative to whole adipose tissue (AT) from the same mouse.
Targeting nuclear receptor NR4A1-dependent adipocyte progenitor quiescence promotes metabolic adaptation to obesity.
No sample metadata fields
View SamplesBrown adipose tissue (BAT) is a thermogenic organ that dissipates stored energy as heat to maintain body temperature in infants and small mammals. This process may also provide protection from development of diet-induced obesity. We found that the bioactive lipid mediator lysophosphatidic acid (LPA) markedly decreases differentiation of cultured primary brown adipocyte precursors, while potent selective inhibitors of the LPA-generating enzyme autotaxin (ATX) promote differentiation. Transgenic mice overexpressing ATX exhibited reduced expression of BAT-related genes in peripheral white adipose tissue and accumulated significantly more fat than wild-type controls when fed a high fat diet. Our results indicate that ATX and its product LPA are physiologically relevant negative regulators of brown fat adipogenesis and suggest that a decrease in peripheral brown adipose tissue results in increased susceptibility to diet-induced obesity in mice.
Autotaxin and its product lysophosphatidic acid suppress brown adipose differentiation and promote diet-induced obesity in mice.
Sex, Age, Specimen part, Treatment
View SamplesCD33-/- and/or TREM2-/- mice were crossed with the 5xFAD mouse model of Alzheimer's disease to generate single and double CD33/TREM2 knock-out mice on 5xFAD background. Transcriptome and gene expression analyses were performed to analyze the impact of CD33 and/or TREM2 knock-out on the transcriptome of microglia in the context of amyloid pathology. The results revealed that CD33 and/or TREM2 knock-out reprogrammed microglial gene expression signatures in 5xFAD mice in an age-dependent manner. Differential gene expression in 5xFAD;CD33-/- microglia depended on the presence of TREM2. These data suggest that TREM2 acts downstream of CD33. Overall design: Microglia were isolated from brains of WT, 5xFAD, 5xFAD;CD33-/-, 5xFAD;TREM2-/-, and 5xFAD;CD33-/-;TREM2-/- mice at 4 and 8 months of age, using FACS sorting for CD11b and CD45. RNA was extracted using the RNeasy Plus Micro Kit (Qiagen). Libraries were prepared using the TruSeq Stranded mRNA LT Prep Kit (Illumina) and sequenced on an Illumina HiSeq 2500 sequencer using single-end 50. Reads were aligned to mouse genome mm10 using the STAR aligner. Read counts for individual genes were obtained using HTSeq.
TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer's Disease.
Age, Cell line, Subject
View SamplesHere we characterize and optimize both systems to increase their utility for preclinical studies. We show that TH-MYCN mice develop tumors in the paraspinal ganglia, but not in the adrenal, with cellular and gene expression patterns similar to human NB. In addition, we present a new ultrasound guided, non-invasive orthotopic xenograft method. This injection technique is rapid, provides accurate targeting of the injected cells and leads to efficient engraftment. We also demonstrate that tumors can be detected, monitored and quantified prior to visualization using ultrasound, MRI and bioluminescence. Finally we develop and test a standard of care chemotherapy regimen. This protocol, which is based on current treatments for neuroblastoma, provides a baseline for comparison of new therapeutic agents.
Preclinical models for neuroblastoma: establishing a baseline for treatment.
Specimen part
View SamplesThe concept of germ layers has been one of the foremost organizing principles in developmental biology, classification, systematics and evolution for 150 years. Of the three germ layers, the mesoderm is found in bilaterian animals but is absent in species in the phyla Cnidaria and Ctenophora, which has been taken as evidence that the mesoderm was the final germ layer to evolve. The origin of the ectoderm and endoderm germ layers, however, remains unclear, with models supporting the antecedence of each as well as a simultaneous origin. Here we determine the temporal and spatial components of gene expression spanning embryonic development for all Caenorhabditis elegans genes and use it to determine the evolutionary ages of the germ layers. The gene expression program of the mesoderm is induced after those of the ectoderm and endoderm, thus making it the last germ layer both to evolve and to develop. Strikingly, the C. elegans endoderm and ectoderm expression programs do not co-induce; rather the endoderm activates earlier, and this is also observed in the expression of endoderm orthologues during the embryology of the frog Xenopus tropicalis, the sea anemone Nematostella vectensis and the sponge Amphimedon queenslandica. Querying the phylogenetic ages of specifically expressed genes reveals that the endoderm comprises older genes. Taken together, we propose that the endoderm program dates back to the origin of multicellularity, whereas the ectoderm originated as a secondary germ layer freed from ancestral feeding functions. Overall design: Two temporal assays of Caenorhabditis elegans embryonic development, starting at the zygote: (a) Embryos collected at fixed (~10 minute) time intervals. (b) Embryo segregates, up to five lines of blastomeres, isolated in reference to mitotic events. There were 184 samples in total, representing 100 distinct data points (50 in each assay).
Spatiotemporal transcriptomics reveals the evolutionary history of the endoderm germ layer.
Subject, Time
View SamplesThe transcriptional regulator Rbpj is involved in T-helper (TH) subset polarization, but its function in Treg cells remains unclear. Here we show that Treg-specific Rbpj deletion leads to splenomegaly and lymphadenopathy despite increased numbers of Treg cells with a polyclonal TCR repertoire. A specific defect of Rbpj-deficient Treg cells in controlling TH2 polarization and B cell responses is observed, leading to the spontaneous formation of germinal centers and a TH2-associated immunoglobulin class switch. The observed phenotype is environment-dependent and can be induced by infection with parasitic nematodes. Rbpj-deficient Treg cells adopt open chromatin landscapes and gene expression profiles reminiscent of tissue-derived TH2-polarized Treg cells, with a prevailing footprint of the transcription factor Gata-3. Taken together, our study suggest that Treg cells require Rbpj to specifically restrain TH2 responses, including their own excessive TH2-like differentiation potential. Overall design: We isolated Treg cells from spleens of affected Treg Rbpj-deficient animals and wildtype counterparts. Total RNA was isolated and subjected to gene expression analysis using RNA sequencing
Rbpj expression in regulatory T cells is critical for restraining T<sub>H</sub>2 responses.
Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The PurR regulon in Escherichia coli K-12 MG1655.
No sample metadata fields
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