As exposure to episodic drought can impinge significantly on forest health and the establishment of productive tree plantations, there is great interest in understanding the mechanisms of drought response in trees. The ecologically dominant and economically important genus Populus, with its sequenced genome, provides an ideal opportunity to examine transcriptome level changes in trees in response to a drought stimulus. The transcriptome level drought response of two commercially important hybrid Populus clones (P. deltoides P. nigra, DN34, and P. nigra P. maximowiczii, NM6) was characterized over a diurnal period using a 4 2 2 completely randomized factorial ANOVA experimental design (four time points, two genotypes, and two treatment conditions) using Affymetrix Poplar GeneChip microarrays. Notably, the specific genes that exhibited changes in transcript abundance in response to drought differed between the genotypes and/or the time of day that they exhibited their greatest differences. This study emphasizes the fact that it is not possible to draw simple, generalized conclusions about the drought response of the genus Populus on the basis of one species, nor on the basis of results collected at a single time point. The data derived from our studies provide insights into the variety of genetic mechanisms underpinning the Populus drought response, and provide candidates for future experiments aimed at understanding this response across this economically and ecologically important genus.
Genotype and time of day shape the Populus drought response.
Age, Specimen part, Treatment
View SamplesVascular smooth muscle cells (VSMCs) respond to biomechanical stretch with specific changes in gene expression which govern the phenotype of these cells. The mechanotransducer zyxin is a
Loss of the mechanotransducer zyxin promotes a synthetic phenotype of vascular smooth muscle cells.
Specimen part, Treatment
View SamplesPurpose:To take a comprehensive effort in characterizing the brain vasculature gene expression upon hyperglycemia. Methods: We extracted mRNA from brain microvasculature fragments isolated from a genetic mouse model of hyperglycemia (Ins2-AKITA) and WT mice and analyzed their transcriptome with RNA sequencing The samples were sequenced on an Illumina HiSeq 2500 sequencer at the SNP&SEQ sequencing facility (Science for Life laboratory (SciLifeLab), Uppsala sequencing node). The reads were aligned to the Ensembl mouse gene assembly (NCBIM37) using Tophat2 software (version 2.0.4). The duplicated reads were removed using the picard tool (version 1.92). To identify the genes significantly enriched in the pericyte samples as compared with microvascular samples, statistical tests were performed using the Cufflinks tool (version 2.2.1) Results: Twenty-three genes were significantly regulated in mutant when compared to WT (False Discovery Rate < 0.05) Overall design: The microvascular RNA from two male heterozygous Ins2-AKITA mice and three littermate wild-type controls were processed and sequenced on the Illumina HiSeq 2500 platform in the sequencing facility in Uppsala University.
Prolonged systemic hyperglycemia does not cause pericyte loss and permeability at the mouse blood-brain barrier.
Sex, Specimen part, Subject
View SamplesWe used microarrays to detail the global programme of gene expression underlying CS1-regulated biological processes including increased cell adhesion and cell proliferation.
CS1 promotes multiple myeloma cell adhesion, clonogenic growth, and tumorigenicity via c-maf-mediated interactions with bone marrow stromal cells.
No sample metadata fields
View SamplesThis analysis focused on identifying factors that protect pre-B cells against DNA double strand break (DSB)-mediated DNA damage stress during pre-B cell differentiation. Differentiation of pre-B cells including immunoglobulin light chain gene recombination were performed by withdrawal of interleukin-7 (IL-7) from IL-7-dependent murine pre-B cells or by inhibition of the BCR-ABL1 kinase activity in BCR-ABL1-transformed pre-B cells.
BCL6 is critical for the development of a diverse primary B cell repertoire.
Specimen part
View SamplesPrecursor B-lineage acute lymphoblastic leukemia (pre-B ALL) can be subdivided into different categories based on genetic abnormalities.
Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function.
Specimen part
View SamplesThe Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. In this study, the tyrosine kinase inhibitor imatinib was used for pharmacological inhibition of BCR-ABL1. Gene expression profiles of Ph+ ALL cell lines were analyzed in response to imatinib treatment.
BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition.
Specimen part, Cell line
View SamplesThe Philadelphia chromosome (Ph) encodes the oncogenic BCR-ABL1 tyrosine kinase, which is present in almost every patient with chronic myeloid leukemia. In this study, the tyrosine kinase inhibitor Imatinib was used for pharmacological inhibition of BCR-ABL1. Gene expression profiles of CML cell lines were analyzed in response to Imatinib treatment.
BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR-ABL1 kinase inhibition.
Specimen part, Cell line
View SamplesBy analyzing 250 astrocyte single cell transcriptomes from adult brain, we provide gene expresssion profile of brain astrocyte Overall design: We chose adult mice about 3 months old and analysed single cells in the brain. We chose a methodology based on fluorescence-activated cell sorting (FACS) into 384-well plates followed by the SmartSeq2 methodology.
Single-cell RNA sequencing of mouse brain and lung vascular and vessel-associated cell types.
Specimen part, Cell line, Subject
View SamplesTo screen for specific circadian outputs that may distinguish the pacemaker in the mammalian suprachiasmatic nucleus (SCN) from peripheral-type oscillators in which the canonical clockworks are similarly regulated in a circadian manner, the rhythmic behavior of the transcriptome in forskolin-stimulated NIH/3T3 fibroblasts was analyzed and compared to that found in the rat SCN in vivo and SCN2.2 cells in vitro. Similar to the scope of circadian gene expression in SCN2.2 cells and the rat SCN, NIH/3T3 fibroblasts exhibited circadian fluctuations in the expression of the core clock genes, Per2, Bmal1 (Mop3), and Cry1 and 323 functionally diverse transcripts (2.6%), many of which were involved in cell communication. Overlap in rhythmically-expressed transcripts among NIH/3T3 fibroblasts, SCN2.2 cells and the rat SCN was limited to these clock genes and four other genes that mediate fatty acid and lipid metabolism or function as nuclear factors. Compared to NIH/3T3 cells, circadian gene expression in SCN oscillators was more prevalent among cellular pathways mediating glucose metabolism and neurotransmission. Coupled with evidence for the rhythmic regulation of the inducible isoform of nitric oxide synthase, the enzyme responsible for the production of nitric oxide, in SCN2.2 cells and the rat SCN but not in fibroblasts, studies examining the effects of a NOS inhibitor on metabolic rhythms in co-cultures containing SCN2.2 cells and untreated NIH/3T3 cells suggest that this gaseous neurotransmitter may play a key role in SCN pacemaker function. Thus, this comparative analysis of circadian gene expression in SCN and non-SCN cells may have important implications in the selective identification of circadian signals involved in the coupling of SCN oscillators and the regulation of rhythmicity in downstream cells or tissues.
Circadian profiling of the transcriptome in NIH/3T3 fibroblasts: comparison with rhythmic gene expression in SCN2.2 cells and the rat SCN.
No sample metadata fields
View Samples