This SuperSeries is composed of the SubSeries listed below.
Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features.
Sex, Age, Specimen part, Disease
View SamplesDifferential gene expression is assessed in substantia nigra and basal ganglia of neurodegenertion with brain iron accumulation cases (BIA) compared to matched normal controls (c).
Brain iron accumulation affects myelin-related molecular systems implicated in a rare neurogenetic disease family with neuropsychiatric features.
Sex, Age, Specimen part, Disease
View SamplesGroup living animals must be able to express different behavior profiles depending on their social status. This implies that the same genotype may translate into different behavioral phenotypes through socially driven differential gene expression. Here we show for the first time that what triggers the switch between status-specific neurogenomic states is not the objective structure of the social interaction but rather the subjects perception of its outcome. For this purpose we had male zebrafish fight either a real opponent or their own image on a mirror. Massive changes in the brain transcriptome were observed in real opponent fighters, which experience either a victory or a defeat. In contrast, mirror fighters, which had no information on fight outcome despite expressing aggressive behavior, failed to activate a neurogenomic response. These results indicate that, even in cognitively simple organisms such as zebrafish, neurogenomic responses underlying changes in social status rely on cognitive appraisal.
Assessment of fight outcome is needed to activate socially driven transcriptional changes in the zebrafish brain.
Specimen part
View SamplesE-cadherin, a protein encoded by the CDH1 gene is the dominant epithelial cell adhesion molecule playing a crucial role in epithelial tissue polarity and structural integrity. The progression of 90% or more carcinomas is believed to be mediated by disruption of normal E-cadherin expression, subcellular localization or function. Despite the strong correlation between E-cadherin loss and malignancy the mechanism through how this occurs is not known in most sporadic and hereditary epithelial carcinomas. Previous works have shown the importance of CDH1 intron 2 sequences for proper gene and protein expression supporting the possibility of these being cis-modulators of E-cadherin expression/function. but when co-expressed it led to reduced cell-cell adhesiveness, increased invasion and angiogenesis. By expression array analysis, IFITM1 and IFI27 levels were found to be increased upon CDH1a overexpression. Importantly, CDH1a was found to be de novo expressed in gastric cancer cell lines when compared to normal stomach.
Transcription initiation arising from E-cadherin/CDH1 intron2: a novel protein isoform that increases gastric cancer cell invasion and angiogenesis.
Specimen part, Cell line
View SamplesThere is an association between transcriptome and the exercise-related phenotype. Peripheral blood cells suffer alterations in the gene expression pattern in response to perturbations caused by exercise. The acute response to endurance activates stress and inflammation, as well as growth and tissue repair responses.
PBMCs express a transcriptome signature predictor of oxygen uptake responsiveness to endurance exercise training in men.
Sex, Specimen part, Disease, Disease stage, Treatment, Subject, Time
View SamplesThe change of genome-wide transcription profiles as a result of Gis1 overexpression is monitored by comparing the transcriptomes isolated from cells where Gis1 overexpression is switched on or off. GIS1 was cloned into pCM190 vector under the control of the tetO7 promoter. The promoter is switched on when there is no doxycycline but off with doxycycline (20ug/ml). Cells were grown in medium with doxycycline, harvested, washes twice in sterile water, resuspended in the same medium with doxycycline (Dox+) or without doxycycline (dox-) and grown for additional 6 hours. Samples were taken for each condition at 3 and 6 hours. Time 0 sample was taken before resuspension.
The transcription activity of Gis1 is negatively modulated by proteasome-mediated limited proteolysis.
Subject, Compound, Time
View SamplesIn order to characterize defense responses not only cytologically, but also on the transcript level, genome-wide sequencing of mRNA isolated from non-infected control leaves and from leaves inoculated either with the WT or with GLS1 overexpressing strains was performed, using Illumina Next Generation Sequencing Technology. In order to identify transcripts specifically induced in leaves infected by ß-1,3-glucan-exposing strains, transcript patterns of leaves inoculated with GLS1 overexpressing PtrpC:GLS1 strains were compared with those of the WT. In PtrpC:GLS1-inoculated leaves, a total of 2179 genes were more than 2.5-fold increased, with many genes known as genes typically up-regulated in PAMP-triggered defense responses. These genes include genes encoding PR proteins enzymes involved in cell wall re-inforcemen, and terpene synthases possibly involved in phytoalexin synthesis. Furthermore, increased transcript abundance of genes encoding serine-threonine receptor-like kinases calmodulin, as well as zinc-finger and WRKY transcription factors have been identified. Other up-regulated genes encode proteins involved in protein degradation, i.e. proteases, ubiquitin ligases, as well as enzymes involved in synthesis of auxin or cytokinin phytohormones. In comparison, 2164 genes were more than 2.5-fold down-regulated in maize leaves infected by PtrpC:GLS1 strains, as compared to WT-infected leaves. Several of the encoded proteins are known susceptibility factors. Forty-six down-regulated genes code for proteins containing iron or manganese, or are involved in uptake of these ions, suggesting major re-arrangement of the redox-status in maize leaves after ß-glucan perception. Overall design: Examination of plant defense responses in maize plants inoculated with 2 different Colletotrichum graminicola strains.
Infection structure-specific expression of β-1,3-glucan synthase is essential for pathogenicity of Colletotrichum graminicola and evasion of β-glucan-triggered immunity in maize.
Age, Subject, Time
View SamplesThe T cell response to Chlamydia genital tract infections in humans and mice is unusual in that the majority of antigen-specific CD8 T cells are not restricted by HLA/MHC class I and therefore have been referred to as “unrestricted” or “atypical”. We previously reported that a subset of unrestricted murine Chlamydia-specific CD8 T cells had an unusual cytokine polarization pattern that included IFN-ɣ and IL-13. For this report, we investigated the transcriptome of Chlamydia-specific CD8ɣ13 T cells, comparing them to Chlamydia-specific multifunctional Tc1 clones using gene expression micro array analysis. The molecular study revealed that CD8ɣ13 polarization included IL-5 in addition to IFN-γ and IL-13. Adoptive transfer studies were performed with Tc1 clone and CD8ɣ13 T cell clones to determine whether either influenced bacterial clearance or immunopathology during Chlamydia muridarum (Cm) genital tract infections. To our surprise, an adoptively transferred CD8ɣ13 T cell clone was remarkably proficient at preventing chlamydia immunopathology while the multifunctional Tc1 clone did not enhance clearance or significantly protect from immunopathology. Mapping studies with MHC class I- and class II-deficient splenocytes showed our previously published Chlamydia-specific CD8 T cell clones are MHC class II-restricted. MHC class II-restricted CD8 T cells may play important roles in protection from intracellular pathogens that limit class I antigen presentation or deplete the CD4 T cell compartment.
A Class II-Restricted CD8γ13 T-Cell Clone Protects During Chlamydia muridarum Genital Tract Infection.
No sample metadata fields
View SamplesThe highly conserved herpesvirus glycoprotein complex, gB/gH-gL, mediates membrane fusion during virion entry and cell-cell fusion. Varicella-zoster virus (VZV) characteristically forms multi-nucleated cells, or syncytia, during the infection of human tissues but little is known about this process. The cytoplasmic domain of VZV gB (gBcyt) has been implicated in cell-cell fusion regulation because a gB[Y881F] substitution causes hyperfusion. The gBcyt regulation is necessary for VZV pathogenesis as the hyperfusogenic mutant gB[Y881F] is severely attenuated in human skin xenografts. In this study, gBcyt regulated fusion was investigated by comparing melanoma cells infected with wild type-like VZV or hyperfusogenic mutants. The gB[Y881F] mutant exhibited dramatically accelerated syncytia formation in melanoma cells caused by fusion of infected cells with many uninfected cells, increased cytoskeleton reorganization and rapid displacement of nuclei to dense central structures when compared to pOka using live cell confocal microscopy. VZV and human transcriptomes were concurrently investigated using RNA-seq to identify viral and cellular responses induced when the gBcyt regulation was disrupted by the gB[Y881F] substitution. The expression of four vital VZV genes, ORF61 and glycoproteins, gC, gE and gI, was significantly reduced at 36 hours post infection for the hyperfusogenic mutants. Importantly, hierarchical clustering demonstrated an association of differential gene expression with dysregulated gBcyt-mediated fusion. A subset of Ras GTPase genes linked to membrane remodeling were upregulated in cells infected with the hyperfusogenic mutants. These data implicate the gBcyt in the regulation gB fusion function that, if unmodulated, triggers cellular processes leading to hyperfusion that attenuates VZV infection. Overall design: Biological duplicates from 3 time points (12, 24 and 36 hours post infection) of uninfected MeWo cells or MeWo cells infected with varicella-zoster virus strain pOka or mutants gB[Y881F], gB[Y920F] or gB[Y881/920F]
Dysregulated Glycoprotein B-Mediated Cell-Cell Fusion Disrupts Varicella-Zoster Virus and Host Gene Transcription during Infection.
Cell line, Subject, Time
View SamplesPublic information is widely available at low cost to animals living in social groups. For instance, bystanders may eavesdrop on signaling interactions between conspecifics and use it to adapt their subsequent behavior towards the observed individuals. This social eavesdropping ability is expected to require specialized mechanisms such as social attention, which selects social information available for learning. To begin exploring the genetic basis of social eavesdropping, we used a previously established attention paradigm in the lab to study the brain gene expression profile of male zebrafish in relation to the attention they have paid towards conspecifics involved or not involved in agonistic interactions. Microarray gene chips were used to characterize their brain transcriptomes based on differential expression of single genes and gene sets. These analyses were complemented by promoter region-based techniques. Using data from both approaches, we further drafted protein interaction networks. Our results suggest that attentiveness towards conspecifics, whether interacting or not, activates pathways linked to neuronal plasticity and memory formation. The network analyses suggested that fos and jun are key players on this response, and that npas4a, nr4a1 and egr4 may also play an important role.
Brain Transcriptomic Response to Social Eavesdropping in Zebrafish (Danio rerio).
Sex, Specimen part, Treatment
View Samples