Fetal liver of E14.5 RNaseh2b KOF and Rnaseh2b wild type embryos was isolated, RNA was extracted and microarray analysis using Affymetrix Mouse 430 2.0 gene chip was performed
Mammalian RNase H2 removes ribonucleotides from DNA to maintain genome integrity.
Specimen part
View SamplesBiallelic defects of the gene encoding for the intracellular enzyme 3’ repair exonuclease (Trex)1 cause Aicardi-Goutières syndrome (AGS), a rare monogenic, lupus-like autoimmune disease, while heterozygous Trex1 loss of function alleles are associated with systemic lupus erythematosus (SLE). Trex1-/- mice develop lethal autoimmune multi-organ inflammation, which results from a chronic type I IFN response triggered by intracellular accumulation of a putative nucleic acid substrate of Trex1. This pathogenic nucleic acid is detected by the broadly, but not ubiquitously, expressed cytosolic DNA sensor cGAS, raising the question whether there are specific cell types that respond to Trex1 deficiency by production of IFN and induce autoimmunity. We generated mice with conditional knock out of the Trex1 gene and demonstrated that loss of Trex1 throughout the hematopoietic system and even selective loss in dendritic cells is sufficient to cause IFN release and autoimmunity. B cells showed no transcriptional response to Trex1 deficiency. Trex1-/- keratinocytes produced IFN but did not induce skin inflammation, whereas loss of Trex1 in cardiomyocytes triggered neither IFN response nor pathology. Trex1-deficient neurons and astrocytes did not release IFN in the CNS. In contrast, mice with selective inactivation of Trex1 in long-living CNS macrophages such as microglia locally produced IFN but did not reproduce the mild encephalitis seen in Trex1-/- mice. Collectively, individual cell types differentially respond to the loss of Trex1 and dendritic cells seem promising candidates for experiments addressing the molecular pathomechanism in Trex1 deficiency. Overall design: We sorted CD19-positive B cells from spleens of Trex1fl/fl CD19-Cre+ and Trex1fl/fl CD19-Cre- mice and isolated total RNA for library construction to perform mRNA deep sequencing.
Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic Autoimmunity.
Specimen part, Subject
View SamplesThis sudy focuses on the identification of transcripts in the shoot phloem of the model plant Arabidopsis thaliana. Transcripts expressed in the phloem tissue (parenchyma cell, companion cell, sieve element) were excised by laser microdissection pressure catapulting (LMPC). These were compared with transcripts isolated from leaf phloem exudates by EDTA-chelation technique. Optimization of sample harvest resulted in RNA of high quality from both sources. Modifications of the RNA amplification procedure obtained RNA of sufficient yield and quality for microarray experiments. Microarrays (Affymetrix, ATH1) hybridized with RNA derived from phloem tissue by LMPC or phloem sap allowed us to differentiate between phloem located and mobile transcript species. The datasets provide a search criterion for phloem-based signals and will facilitate reverse genetic studies and forward genetic screens for phloem and long distance RNA signaling mutants.
Identification of Arabidopsis thaliana phloem RNAs provides a search criterion for phloem-based transcripts hidden in complex datasets of microarray experiments.
No sample metadata fields
View SamplesMetastasis to lymph nodes is an early and prognostically important event in the progression of many human cancers, and is associated with expression of vascular endothelial growth factor-D (VEGF-D). Changes to lymph node vasculature occur during metastasis, and may establish a metastatic niche capable of attracting and supporting tumor cells.
A role for bone morphogenetic protein-4 in lymph node vascular remodeling and primary tumor growth.
Sex, Specimen part
View SamplesRay cells were enriched from wood samples of poplar (Populus x canescens) by LMPC and transcripts monitored by poplar whole genome microarrays. Results provided insight into molecular processes during the transition from dormancy to flowering in early spring in contrast to the active growth phase in summer.
Poplar wood rays are involved in seasonal remodeling of tree physiology.
No sample metadata fields
View SamplesA three-dimensional chromatin state underpins the structural and functional basis of the genome by bringing regulatory elements and genes into close spatial proximity to ensure proper, cell-type specific gene expression profiles. Here, we perform HiC chromosome conformation, ChIP-seq and RNA-seq to investigate how the three-dimensional organization of the cancer genome is disrupted in the context of epigenetic remodelling and atypical gene expression programs. Overall design: Hi-C, ChIP-seq and RNA-seq were conducted in three human prostate cell lines: normal prostate epithelial cells (PrEC) and prostate cancer cells (PC3 and LNCaP).
Three-dimensional disorganization of the cancer genome occurs coincident with long-range genetic and epigenetic alterations.
No sample metadata fields
View SamplesMitochondrial dysfunction has been directly or indirectly implicated in the pathogenesis of a number of neurodegenerative disorders including Parkinson's disease, Alzheimer's disease and Amyotrophic Lateral Sclerosis (ALS). We used exon-sentive microarrays to characterize the responses to different mitochondrial perturbations in cellular models. We examined human SH-SY5Y neuroblastoma cells treated with paraquat, a neurotoxic herbicide which both catalyzes the formation of reactive oxygen species (ROS) and induces mitochondrial damage in animal models, and SH-SY5Y cells stably expressing the mutant SOD1(G93A) protein, one of the genetic causes of ALS. We identified a common set of genes that have a deregulated transcription and alternative splicing in both models. Noticeably, pathway analysis revealed that the expression of a subset of genes involved in neuritogenesis and axon guidance is perturbed, suggesting that alterations of axonal function may descend directly from mitochondrial damage and be responsible for neurodegenerative conditions.
Mutant SOD1 and mitochondrial damage alter expression and splicing of genes controlling neuritogenesis in models of neurodegeneration.
Cell line
View SamplesWhole-genome profiling of SH-SY5Y cells was done on neuroblastoma SH-SY5Y stably transfected with cDNAs coding for SOD1WT or the mutant SOD1(G93A) protein.
Mutant SOD1 and mitochondrial damage alter expression and splicing of genes controlling neuritogenesis in models of neurodegeneration.
Cell line
View SamplesHuman SH-SY5Y neuroblastoma cells treated with paraquat, a neurotoxic herbicide which both catalyzes the formation of reactive oxygen species (ROS) and induces mitochondrial damage in animal models was profiled using Affimetrix Exon 1.0 ST GeneChips
Mutant SOD1 and mitochondrial damage alter expression and splicing of genes controlling neuritogenesis in models of neurodegeneration.
Cell line
View SamplesThe aim was to identify genes that were commonly influenced by a siRNA targeting PRKCD in breast cancer cell lines.
Down Regulation of CLDND1 Induces Apoptosis in Breast Cancer Cells.
Cell line, Treatment
View Samples