Magnaporthe oryzae is the causative agent of the rice blast, the most relevant rice disease worldwide. To date expression analysis on rice infected with Magnaporthe oryzae have been carried out only with the strains FR13 (leaf) and Guy 11 (root). However different strains of Magnaporthe are present in the environment leading to different rice responses at molecular level. To gain more insight on the unknown molecular mechanisms activated by different Magnaporthe strains during rice defense, a global expression analysis was performed by using the GeneChip Rice Genome Array.
OsWRKY22, a monocot WRKY gene, plays a role in the resistance response to blast.
Specimen part
View SamplesPowdery mildew is a very common plant disease and only few plants are immune. Host interactions have been identified and characterized for the pathosystems barley-B. graminis f. sp. tritici (Bgt) and wheat-B. graminis f. sp. hordei (Bgh), whereas no data are reported about powdery mildew and nonhost plants, such as rice. On the other hand rice nonhost resistance is widely unexploited and only few expression data are available. To characterize rice response during nonhost interaction with Bgh, a global expression analysis was performed by using the GeneChip Rice Genome Array.
OsWRKY22, a monocot WRKY gene, plays a role in the resistance response to blast.
Specimen part
View SamplesWe are using the ACI rat model of 17beta-estradiol induced mammary cancer to define the mechanisms through which estrogens contribute to breast cancer development; identify and functionally characterize the genetic variants that determine susceptibility; and define the hormone-gene-environment interactions that influence development of mammary cancer in this physiologically relevant rat model. Female ACI rats are uniquely susceptible to development of mammary cancer when treated continuously with physiologic levels of 17beta-estradiol. Induction of mammary cancer in female ACI rats occurs through a mechanism that is largely dependent upon estrogen receptor-alpha. Interval mapping analyses of progeny generated in intercrosses between susceptible ACI rats and resistant Brown Norway (BN) rats revealed seven quantitative trait loci (QTL), designated Emca3 (Estrogen-induced mammary cancer) through Emca9, each of which harbors one or more genetic determinants of mammary cancer susceptibility. Genes that reside within Emca8 on RNO5 and were differentially expressed between 17beta-estradiol treated ACI and ACI.BN-Emca8 congenic rats were identified as Emca8 candidates.
Mapping of three genetic determinants of susceptibility to estrogen-induced mammary cancer within the Emca8 locus on rat chromosome 5.
Sex, Age, Specimen part
View SamplesThis study demonstrates that siRNA off-targets (e.g. 3'UTR off-targets), can be significantly reduced when cells are treated with a relatively low dose of siRNA (e.g. 1nM) that is sufficient to effectively silence the intended target.
siRNA off-target effects can be reduced at concentrations that match their individual potency.
Cell line
View SamplesTight regulation of hematopoietic stem cell (HSC) homeostasis is essential for life-long hematopoiesis, for preventing blood cancers and for averting bone marrow failure. The underlying mechanisms are incompletely understood. Here, we identify production of inositol-tetrakisphosphate (IP4) by inositoltrisphosphate 3-kinase B (ItpkB) as essential for HSC quiescence and function. Young ItpkB-/- mice accumulated phenotypic HSC and showed extramedullary hematopoiesis. ItpkB-/- HSC were less quiescent and proliferated more than wildtype controls. They downregulated quiescence and stemness associated mRNAs, but upregulated activation, oxidative metabolism, protein synthesis and lineage associated transcripts. Although they showed no significant homing defects, ItpkB-/- HSC had a severely reduced competitive long-term repopulating potential. Aging ItpkB-/- mice lost hematopoietic stem and progenitor cells and died with severe anemia. Wildtype HSC normally repopulated ItpkB-/- hosts, incidating a HSC-intrinsic ItpkB requirement. ItpkB-/- HSC had reduced cobblestone-area forming cell activity in vitro and showed increased stem-cell-factor activation of the phosphoinositide 3-kinase (PI3K) effector Akt, reversed by exogenous provision of the known PI3K/Akt antagonist IP4. They also showed transcriptome changes consistent with hyperactive Akt/mTOR signaling. Thus, we propose that ItpkB ensures HSC quiescence by limiting cytokine-induced PI3K signaling in HSC. Overall design: For each of 3 replicate ItpkB-/- or wt samples, we enriched Lin- cells from BM of 4 pooled age-matched mice with Rapidspheres (Stemcell Technologies), FACS-sorted =10,000 LSK CD34-CD150+CD48-Flk2- LT-HSC into lysis buffer and prepared RNA with RNeasy Micro kits (Quiagen). RNA sequencing was done using an Illumina HISeq Analyzer 2000, Casava v1.8.2 genome analyzer pipeline, TopHat v1.4.1/Bowtie2 genome alignment and Partek v6.6 mRNA annotation software. Statistical analyses were done with edgeR (Bioconductor package), excluding genes with false discovery rates >0.15, fold-change magnitudes =1.4 and log2(counts per million) =4 to avoid undefined values and the poorly defined log fold-changes for low counts close to 0. Unsupervised clustering of 441 significantly changed genes was done with dChip using rank correlation and a centroid linkage method. Scatter plots were generated in Spotfire. GSEA was performed with gene set permutation, using gene sets from MSigDB (www.broadinstitute.org/gsea/msigdb/index.jsp) or manually curated from, excluding genes without HUGO approved symbols
IP3 3-kinase B controls hematopoietic stem cell homeostasis and prevents lethal hematopoietic failure in mice.
No sample metadata fields
View SamplesHuman bone marrow is a complex, diversified and well-organized hematopoietic network changing composition with age. The purpose of this study was to analyze variations in relative precursor B cell abundance in bone marrow with age by means of global gene expression profiling. RNA was isolated from composite bone marrow from 25 healthy children, adolescents and adults age 2 months to 28 years. As reference transcript for precursor B cells we used recombination activating gene RAG1 exploring the data for other transcripts showing the same profile as RAG1 with age. We identified 54 genes with correlated expression profiles to RAG1 (r 0.9, p = 0), characterized by high expression at 3 - 20 months followed by a fast decline to lower signal levels maintained until early adulthood. Immunophenotyping from a similar healthy age-matched cohort (n = 37) showed a comparable decrease of precursor B cells. Of the 54 genes 15 were characteristically B cell associated representing cell surface molecules (CD19, CD72, CD79A, CD79B, CD180, IGL@, IGLL1, VPREB1, VPREB3), a signal transduction molecule (BLNK) and transcription factors (DNTT, EBF1, PAX5, POU2AF1, RAG2). Of the remaining transcripts some may represent novel B cell transcripts or genes involved in control of B cells.
Striking decrease in the total precursor B-cell compartment during early childhood as evidenced by flow cytometry and gene expression changes.
No sample metadata fields
View SamplesEstrogen plays an important role in the regulation of vascular tone and in the pathophysiology of cardiovascular disease. Physiological effects of estrogen are mediated through estrogen receptors alpha (ERalpha) and beta (ERbeta), which are both expressed in vascular smooth muscle and endothelial cells. However, the molecular pathways mediating estrogen effects in blood vessels are not well defined. We have performed gene expression profiling in the mouse aorta to identify comprehensive gene sets the expression of which is regulated by long-term (1 wk) estrogen treatment. The ER subtype dependence of the alterations in gene expression was characterized by parallel gene expression profiling experiments in ERalpha-deficient [ERalpha knockout (ERalphaKO)] and ERbeta-deficient (ERbetaKO) mice.
Estrogen receptors alpha and beta mediate distinct pathways of vascular gene expression, including genes involved in mitochondrial electron transport and generation of reactive oxygen species.
No sample metadata fields
View SamplesKATP opposes depolarization of cells in the heart, smooth muscle, and other tissues by permitting the efflux of potassium ions and this efflux is evidently required to prevent unopposed vasoconstriction and insufficiency of coronary artery blood flow triggered by one or more cytokines induced in response to LPS. The cytokine(s) involved must elicit a dysfunctional response in the Kir6.1-deficient environment, and to gain further insight into the effects of the mutation, we examined the transcriptional status of whole heart, isolated from normal C57BL/6J mice or KcnJ8Md/Md mice, before and after injection of 1 g of LPS
ATP-sensitive potassium channels mediate survival during infection in mammals and insects.
No sample metadata fields
View SamplesA mouse model for human small cell lung carcinoma (SCLC) has been developed based on evidence in human tumors that the tumor suppressor functions of RB and p53 are defective in more than 90% of SCLC cases. We also developed another mouse model also combines loss of p130 (Rbl2), an RB-related gene, with deletion of RB and p53. These two mouse tumors were shown to closely resemble human SCLC.
Loss of p130 accelerates tumor development in a mouse model for human small-cell lung carcinoma.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Cytomegalovirus infection drives adaptive epigenetic diversification of NK cells with altered signaling and effector function.
Specimen part, Subject
View Samples