A fundamental question in biology is how gene expression is regulated to give rise to a phenotype. However, transcriptional variability is rarely considered and could influence the relationship between genotype and phenotype. It is known in unicellular organisms that gene expression is often noisy rather than uniform and has been proposed to be beneficial when environmental conditions are unpredictable. However, little is known about transcriptional variability in multicellular organisms. Using transcriptomic approaches, we analysed gene expression variability over a 24 hours time-course between individual Arabidopsis thaliana plants growing in stable conditions. We identified hundreds of genes that exhibit high inter-individual variability and found that many are involved in environmental responses. We also identified factors that might facilitate gene expression variability, such as gene size, the number of transcription factors regulating a gene and the chromatin environment. These results will bring a new light into the impact of transcriptional variability in gene expression regulation in plants. Overall design: RNA-seq were generated for 14 individual seedlings for each of the 12 following time points: ZT2, ZT4, ZT6, ZT8, ZT10, ZT12 (just before dusk), ZT14, ZT16, ZT18, ZT20, ZT22 and ZT24 (just before dawn).
Widespread inter-individual gene expression variability in <i>Arabidopsis thaliana</i>.
Specimen part, Subject, Time
View SamplesThe Oscillation Zone (OZ) of unsynchronized roots was disected and divided into an upper (OZ2) and lower (OZ1) half .
Oscillating gene expression determines competence for periodic Arabidopsis root branching.
Age, Specimen part
View SamplesAnalysis between two different types of T cells
Comparison of Invariant NKT Cells with Conventional T Cells by Using Gene Set Enrichment Analysis (GSEA).
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Intrinsic self-DNA triggers inflammatory disease dependent on STING.
Specimen part
View SamplesInflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies.
Intrinsic self-DNA triggers inflammatory disease dependent on STING.
Specimen part
View SamplesInflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies.
Intrinsic self-DNA triggers inflammatory disease dependent on STING.
Specimen part
View SamplesTranslational control is critical for early Drosophila embryogenesis and is exerted mainly at the gene-specific level.
Global analyses of mRNA translational control during early Drosophila embryogenesis.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
STING-Dependent Signaling Underlies IL-10 Controlled Inflammatory Colitis.
Specimen part
View SamplesThat commensal bacteria can influence intestinal inflammation has been observed using other models of chronic colitis. Loss of IL-10, a major immunosuppressive cytokine, induces spontaneous colitis in mice. The incidence of spontaneous polyp formation in IL-10-deficient mice was also completely eliminated in the absence of STING
STING-Dependent Signaling Underlies IL-10 Controlled Inflammatory Colitis.
Specimen part
View SamplesMyD88 may play a direct role in STING-dependent signaling, or alternatively that STING-dependent pro-inflammatory cytokines may require downstream MyD88-dependent signaling to exert their effect.
STING-Dependent Signaling Underlies IL-10 Controlled Inflammatory Colitis.
Specimen part
View Samples