TH-MYCN transgenic (Tg) mice are the model for neuroblastoma. One of the sympathetic ganglia is the origin of neuroblastoma in those mice. The tumor incidences of homozygotes and hemizygotes are 100% and 70-80%, respectively.
Inactivation of SMC2 shows a synergistic lethal response in MYCN-amplified neuroblastoma cells.
Specimen part
View SamplesTo examine irreversible changes in the developing brain following seizures, juvenile inbred mice were intraperitoneally injected with kainate and nicotine.
Increased expression of the lysosomal protease cathepsin S in hippocampal microglia following kainate-induced seizures.
No sample metadata fields
View Samplesaffy_seed_kinetic_wheat - affy_seed_kinetic_wheat - Study gene expression during the grain developmental -The aim of the study is to identify the genes that are differentially expressed during the grain development in wheat.-Study gene expression during the grain developmental Sample at 100 degree days, year 2004 and 2006 Sample at 200 degree days, year 2004 and 2006 Sample at 250 degree days, year 2004 and 2006 Sample at 300 degree days, year 2004 and 2006 Sample at 400 degree days, year 2004 and 2006
RNA-seq in grain unveils fate of neo- and paleopolyploidization events in bread wheat (Triticum aestivum L.).
No sample metadata fields
View SamplesWe performed RNA-Seq on PHF21A-deficient patient-dervied lymphoblasts as well as two unaffected individuals. Overall design: We performed RNA-Seq from patient-derived lymphoblast cells. Libraries were polyA-selected and strand-specific according to the protocol described in PMID: 25607527
Transcriptome Analysis Revealed Impaired cAMP Responsiveness in PHF21A-Deficient Human Cells.
Sex, Specimen part, Disease stage, Subject
View SamplesPurpose: We purified spinal cord microglia utilizing percoll gradients and magnetic beads, followed by transcriptome profiling (RNA-seq) to define microglia expression profiles against other neural, immune cell-types. We next observed how the microglai transcriptomes change during activation in the SOD1-G93A mouse model of motor neuron degeneration at 3 timepoints. We also compared these profiles with that induced by LPS injection. Results and conclusions: ALS microglia were found to differ substantially from those activated by LPS and from M1/M2 macrophages by comparison with published datasets. These ALS microglia showing substantial induction of a "neurodegeneration-tailored phenotype", with induction of lysosomal, RNA splicing, and Alzheimer''s disease pathway genes. Overall they express a mixture of neuroprotective and neurotoxic factors during activation in ALS mice, showing that neuro-immune activation in the spinal cord is a double-edged sword. We also detected the transcriptional nature of surface marker expression in microglia (CD11b, CD86, CD11c), and substantial T-cell microglia cross-talk using correlative microglia transcriptome/FACS analysis. Overall design: 42 total RNA samples from purified spinal cord microglia were subjected to paired-end RNA-sequencing. Parallel flow cytometry data was collected from the same spinal cords.
A neurodegeneration-specific gene-expression signature of acutely isolated microglia from an amyotrophic lateral sclerosis mouse model.
Specimen part, Disease, Disease stage, Subject
View SamplesAmyotrophic Lateral Sclerosis (ALS) results from the selective and progressive degeneration of motor neurons. Although the underlying disease mechanisms remain unknown, glial cells have been implicated in ALS disease progression. Here we examine the effects of glial cell/motor neuron interactions on gene expression, using the hSOD1G93A mouse model of ALS. We detect striking cell autonomous and non-autonomous changes in gene expression in co-cultured motor neurons and glia, revealing that the two cell types profoundly affect each other. In addition, we found a remarkable concordance between the cell culture data, expression profiles of whole spinal cords, and of acutely isolated spinal cord cells, during disease progression in the G93A mouse model, providing validation of the cell culture approach. Bioinformatics analyses identified changes in the expression of specific genes and signaling pathways that may contribute to motor neuron degeneration in ALS, among which are TGF-b signaling pathways. Overall design: RNA-seq profiles of: 1) 43 Sandwich culture samples at 3 different time points (3, 7 and 14 days), in duplicate, in different combinations of genetic background WT/SOD1_G93A mutant glia and WT/SOD1_G93A mutant neurons; 2) 16 spinal cord samples at 4 different time points, WT and SOD1_G93A mutant.
Intricate interplay between astrocytes and motor neurons in ALS.
Sex, Subject, Time
View SamplesThe adipocytes functions as a central organ in the regulation of metabolic homeostasis. Factors which contribute to the adipocyte differentiation and function would be the promising targets to combat the obesity and associated metabolic disorders. The activating transcription factor 7 (ATF7), a stress-responsive chromatin regulator, has recently been shown to be involved in the energy metabolism; however, the underlying mechanisms are still unknown. Here, we show that ATF7 is required for adipocyte differentiation and it interacts with histone dimethyltransferase G9a in adipocyte to repress the interferon-stimulated genes (ISGs) expression, which suppresses adipogenesis. Ablation of ATF7 promotes the beige biogenesis and browning of inguinal white adipose tissue (iWAT). ATF7 binds to the transcription regulatory regions of Ucp1 gene, and silences it by maintaining the histone H3K9 dimethylation level. These results establish the multifunction of ATF7 in adipocyte and provide molecular insights into the epigenetic control of development and function of adipose tissues. Overall design: Beige adipocytes derived from WT and ATF7 KO inguinal WAT preadipocytes with rosiglitazone treatment, in duplicate; white adipocytes derived from WT and ATF7 KO inguinal WAT preadipocytes without rosiglitazone treatment, in duplicate; beige adipocytes derived from control and ATF7 overexpressing C3H10t1/2 with rosiglitazone treatment, in duplicate, using NextSeq500 Illumina.
The Transcription Factor ATF7 Controls Adipocyte Differentiation and Thermogenic Gene Programming.
Specimen part, Cell line, Subject
View SamplesGlycinebetaine-induced water-stress tolerance in codA-expressing transgenic indica rice is associated with up-regulation of several stress responsive genes.
Glycinebetaine-induced water-stress tolerance in codA-expressing transgenic indica rice is associated with up-regulation of several stress responsive genes.
Specimen part
View SamplesRsp5 is an essential and multi-functional E3 ubiquitin ligase in Saccharomyces cerevisiae. We previously isolated the Ala401Glu rsp5 mutant, which is hypersensitive to various stresses. To understand the function of Rsp5 in stress responses, suppressor genes whose overexpression allows rsp5A401E cells to grow at high temperature were screened. The KIN28 and POG1 genes, encoding a subunit of the transcription factor TFIIH and a putative transcriptional activator, respectively, were identified as multicopy suppressors of not only high temperature but also LiCl stresses. The overexpression of Kin28 and Pog1 in rsp5A401E cells caused an increase in the transcriptional level of some stress proteins when exposed to temperature up-shift. DNA microarray analysis under LiCl stress revealed that the transcriptional level of some proteasome components was increased in rsp5A401E cells overexpressing Kin28 or Pog1. These results suggest that the overexpression of Kin28 and Pog1 enhances the protein refolding and degradation pathways in rsp5A401E cells.
Overexpression of two transcriptional factors, Kin28 and Pog1, suppresses the stress sensitivity caused by the rsp5 mutation in Saccharomyces cerevisiae.
No sample metadata fields
View SamplesIn sexual reproduction, a proper communication and cooperation between male and female organs and tissue are essential for male and female gametes to unite. In flowering plants, female sporophytic tissues and gametophyte direct a male pollen tube towards an egg apparatus, which consists of an egg cell and two synergid cells. The cell-cell communication between the pollen tube and the egg apparatus, such as the reception of a signal from the egg apparatus at the pollen tube, makes the tip of pollen tube rapture to release the sperm cell. To isolate male factors involved in the interaction between a pollen tube and an egg apparatus, we focused on receptor-like kinases (RLKs), which are extensively diversified in the flowering plant lineage to comprise a large monophyletic gene family. Approximately 620 members were found in the Arabidopsis thaliana genome. Expression patterns of 558 RLKs were analyzed using an Affymetrix ATH1 microarray of A. thaliana. We focused on two RLKs, ANXUR1 (ANX1) and ANXUR2 (ANX2), and characterized their function. Here we report that pollen tubes of anx1/anx2 ruptured before arriving at the egg apparatus, suggesting that ANX1 and ANX2 are male factors controlling pollen tube behavior with directing rupture at proper timing. Furthermore, ANX1 and ANX2 were the most closely related paralogs to a female factor FERONIA/SIRENE controlling pollen tube behavior expressed in synergid cells. Our finding shows that the coordinated behaviors of female and male reproductive apparatuses are regulated by the sister genes, whose duplication might play a role in the evolution of fertilization system in flowering plants.
ANXUR1 and 2, sister genes to FERONIA/SIRENE, are male factors for coordinated fertilization.
No sample metadata fields
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