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SRP101622
Zea mays
15 Downloadable Samples
Illumina HiSeq 1500
Description
UV-B radiation affects leaf growth in a wide range of species. In this work, we demonstrate that UV-B levels present in solar radiation inhibits maize leaf growth without causing any other visible stress symptoms, including accumulation of DNA damage. We conducted kinematic analyses of cell division and expansion to understand the impact of UV-B radiation on these cellular processes. Our results demonstrate that the decrease in leaf growth is a consequence of a reduction in cell production, and a shortened growth zone (GZ) in UV-B irradiated leaves. To determine the molecular pathways involved in UV-B inhibition of leaf growth, we performed RNA sequencing on isolated GZ tissues of control and UV-B exposed plants. Our results show a link between the observed leaf growth inhibition and the expression of specific cell cycle and developmental genes, including Growth Regulating Factors (GRFs) and transcripts for proteins participating in different hormone pathways. Overall design: Factorial design with two factors: Treatment (control vs UV-B) x Zone I (0-1cm from base of the leaf), 2 (1-2cm from base of the leaf) and 3 (2-3cm from base of the leaf), 3 replicates
Publication Title
UV-B Inhibits Leaf Growth through Changes in Growth Regulating Factors and Gibberellin Levels.
Alternate Accession IDs
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina Genome Analyzer IIx
Description
After co-evolving with humans, its only major host, Mycobacterium tuberculosis (Mtb) restrains immune responses well enough to escape eradication, yet elicits enough immunopathology to ensure its transmission. Here, we provide evidence that this balance is regulated in part by a previously uncharacterized, cytosolic, membrane-associated protein with a novel structural fold, encoded by the Mtb gene rv0431. The protein acts by regulating the quantity and quality of Mtb-derived membrane vesicles bearing TLR2 ligands, including the lipoproteins LpqH and SodC. We propose that rv0431 be named virR (vesiculogenesis and immune response regulator). To our knowledge, VirR is the first bacterial protein identified to regulate vesiculogenesis. Overall design: Transcriptome sequencing of mouse macrophages uninfected, infected with WT Mtb, or infected with rv0431 mutant Mtb.
Publication Title
Genetic regulation of vesiculogenesis and immunomodulation in Mycobacterium tuberculosis.
Alternate Accession IDs
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Mus musculus
- 24 Downloadable Samples
Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Human infection with Cryptococcus neoformans (Cn), a prevalent fungal pathogen, occurs by inhalation and deposition in the lung alveoli of infectious particles. The subsequent host pathogen interaction is multifactorial and can result either in eradication, latency or extra-pulmonary dissemination. Successful control of Cn infection is dependent on host macrophages as shown by numerous studies. However in vitro macrophages display little ability to kill Cn. Recently, we reported that ingestion of Cn by macrophages induces early cell cycle progression that is subsequently followed by mitotic arrest, an event that almost certainly reflects damage to the host cell. The goal of the present work was to understand macrophage pathways affected by Cn toxicity. Infection of J774.16 macrophage-like cell line macrophages by Cn in vitro was associated with changes in gene pattern expression. Concomitantly we observed depolarization of macrophage mitochondria and alterations in protein translation rate. Our results indicate that Cn infection impairs multiple host cellular functions. Therefore we conclude Cn intracellular residence in macrophages undermines the health of these critical phagocytic cells interfering with their ability to clear the fungal pathogen.
Publication Title
Macrophage mitochondrial and stress response to ingestion of Cryptococcus neoformans.
Alternate Accession IDs
Sample Metadata Fields
Specimen part, Cell line, Time
View Samples- Mus musculus
- 15 Downloadable Samples
- Illumina HiSeq 2500
Description
Using a mouse model overexpressing human SNCA and profiling the striatal transcriptome, we assessed gene-environment interactions to reveal perturbations in gene expression and their modulation through chronic unpredictable mild stress (CUMS) exposure. Overall design: Using a 2x2 factorial design, we cross-compared a line of transgenic mice overexpressing human SNCA with wildtype animals, and the effects of chronic unpredictable mild stress (CUMS) with standard housing conditions. Employing RNA-seq, we profiled gene expression in the striatum of 6-month-old female animals.
Publication Title
Distinct Stress Response and Altered Striatal Transcriptome in Alpha-Synuclein Overexpressing Mice.
Alternate Accession IDs
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 13 Downloadable Samples
- Illumina HiSeq 2500
Description
Using a mouse model overexpressing human SNCA and profiling the striatal transcriptome, we assessed gene-environment interactions to reveal perturbations in gene expression and their modulation through chronic unpredictable mild stress (CUMS) exposure. Overall design: Using a 2x2 factorial design, we cross-compared a line of transgenic mice overexpressing human SNCA with wildtype animals, and the effects of chronic unpredictable mild stress (CUMS) with standard housing conditions. Employing RNA-seq, we profiled gene expression in the striatum of 6-month-old female animals.
Publication Title
Distinct Stress Response and Altered Striatal Transcriptome in Alpha-Synuclein Overexpressing Mice.
Alternate Accession IDs
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Mus musculus
- 16 Downloadable Samples
- Illumina HiSeq 2500
Description
Using a mouse model overexpressing human SNCA and profiling the hippocampal transcriptome, we assessed gene-environment interactions to reveal perturbations in gene expression and their modulation through long-term enriched environment (EE) exposure. We observed that EE prevented perturbations of genes attributed to neuronal and glial cell types and linked to glutamate signaling, calcium homeostasis, inflammation, and related processes of SNCA biology. Cluster and promoter analyses suggested driver genes that specifically responded to the EE, and pointed to a pivotal role of Egr1 to have hierarchically activated other drivers. We suggest a model in which EE-induced driver genes prevent and counter-balance perturbations of SNCA overexpression, restoring a largely normalized gene expression profile and system state. Overall design: Using a 2x2 factorial design, we cross-compared a line of transgenic mice overexpressing human SNCA with wildtype animals, and the effects of a long-term EE with standard housing conditions. Employing RNA-seq, we profiled gene expression in the hippocampus of 12-month-old female animals.
Publication Title
Environmental Enrichment Prevents Transcriptional Disturbances Induced by Alpha-Synuclein Overexpression.
Alternate Accession IDs
Sample Metadata Fields
Age, Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 4 Downloadable Samples
- Illumina Genome Analyzer IIx
Description
Solid tumors are less oxygenated than normal tissues, and for this reason the cancer cells have developed several molecular mechanisms of adaptation to hypoxic environment. Moreover, his poor oxygenation is a major indicator of an adverse prognosis and leads resistance to standard anticancer treatment. Previous reports from this laboratory showed an involvement of Che-1/AATF (Che-1) in cancer cell survival under stress conditions, and on the basis of these observations, we hypothesized that Che-1 might have a role in the response of cancer cells to hypoxia. Methods: The human colon adenocarcinoma cell line HCT116 depleted or not for Che-1 by siRNA, was subjected to normoxic and hypoxic conditions to perform studies about the role of this protein in metabolic adaptation and cell proliferation. The expression of Che-1 under normoxia or hypoxia was detected using western blot assays; cell metabolism was assessed by NMR spectroscopy and functional assays. Further molecular studies were performed by RNA seq, qRT-PCR and ChIP analysis. Results: In this paper we report that Che-1 expression is required for the adaptation of the cells to hypoxia, playing and important role in metabolic modulation. Indeed, Che-1 depletion impacted on glycolysis by altering the expression of several genes involved in the response to hypoxia by modulating the levels of HIF-1alpha. Conclusions: These data demonstrate a novel player in the regulation of a HIF1alpha in response to hypoxia. We found that the transcriptional down-regulation of a members of E3 ubiquitin ligase family SIAH2 by Che-1, produces a failure in the degradation by the hydroxylase PHD3 with a decrease in HIF-1alpha levels during hypoxia. Overall design: The human colon adenocarcinoma cell line HCT116 depleted or not for Che-1 by siRNA was profiled for mRNA high-troughput sequencing (RNA-seq)
Publication Title
Che-1 sustains hypoxic response of colorectal cancer cells by affecting Hif-1α stabilization.
Alternate Accession IDs
Sample Metadata Fields
Cell line, Subject
View Samples- Mus musculus
- 7 Downloadable Samples
- Affymetrix Mouse Gene 2.0 ST Array (mogene20st)
Description
As part of a study of the role of the aryl hydrocarbon receptor (Ahr) in maintenance and senescence of hematopoietic stem cells (HSC), global gene expression profiling was done with HSC isolated from Ahr-knockout and wild-type mice. HSC from young-adult (8 wk old) AhR-KO mice had changes in expression of many genes related to HSC maintenance, consistent with the phenotype observed in aging Ahr-KO mice: decreased survival rate, splenomegaly, increased circulating white blood cells, hematopoietic cell accumulation in tissues, anemia, increased numbers of stem/progenitor and lineage-committed cells in bone marrow, decreased erythroid progenitor cells in bone marrow, and decreased self-renewal capacity of HSC.
Publication Title
Loss of aryl hydrocarbon receptor promotes gene changes associated with premature hematopoietic stem cell exhaustion and development of a myeloproliferative disorder in aging mice.
Alternate Accession IDs
Sample Metadata Fields
Specimen part
View Samples- Mus musculus, Homo sapiens
- 12 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Regional localization within the bone marrow influences the functional capacity of human HSCs.
Alternate Accession IDs
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Demonstration of hematopoietic stem cells (HSCs) was first shown in the mouse and was dependent on recipient bone marrow (BM) to support in vivo multilineage hematopoietic reconstitution, thereby illustrating non-cell-autonomous requirements for HSC functions. Murine studies have defined microanatomic compartments in the BM comprised of osteoblasts, mesenchymal cells, subsets of vasculature, and innervating neural cells functioning as an HSC-supportive niche. Despite the potential clinical applications, analyses of putative HSCs in the BM of humans has not been examined. Here, using human bone biopsies, we provide evidence of HSC propensity to endosteal regions of Trabecular Bone Area (TBA). Independent of phenotypic definitions based on prospective isolation, functional studies indicate that human HSCs residing in the TBA of human and transplanted recipients had superior regenerative and self-renewal capacity and are molecularly distinct to those repopulating the Long Bone Area (LBA). Consistent with the non-cell-autonomous nature of HSC function, osteoblasts in the TBA possess unique characteristics and expressed a key network of factors including those involving Notch activity which could regulate TBA vs. LBA location of human HSCs in vivo. Our study illustrates that human-mouse xenografts provide a surrogate to indigenous human HSC in the BM, and demonstrates that BM architecture plays a critical role in defining functional properties of human HSCs.
Publication Title
Regional localization within the bone marrow influences the functional capacity of human HSCs.
Alternate Accession IDs
Sample Metadata Fields
Specimen part
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