Plants respond to changes in the red:far red ratio (R:FR) of incident light. A reduction in this ratio (increase in FR) results in the Shade Avoidance Response (SAR) with associated changes in gene expression. The Phyotchrome-Interacting Factors (PIFs) are bHLH transcription factors known to be involved in the SAR. An analysis of changes in gene expression in WT and quadruple pif1pif3pif4pif5 (pifq; Leivar et al., 2008 (PMID 19920208)) mutant seedlings in response to an increase in FR should identify primary targets of PIF signaling.
Dynamic antagonism between phytochromes and PIF family basic helix-loop-helix factors induces selective reciprocal responses to light and shade in a rapidly responsive transcriptional network in Arabidopsis.
Specimen part
View SamplesLight initiates the seedling deetiolation transition by promoting major changes in gene expression mainly regulated by phytochrome (phy) photoreceptors. During the initial dark-to-light transition, phy photoactivation induces rapid changes in gene expression that eventually lead to the photomorphogenic development. Recent reports indicate that this process is achieved by phy-induced degradation of Phy-Interacting bHLH transcription Factors (PIFs) PIF1, PIF3 PIF4 and PIF5, which are partly redundant constitutive repressors of photomorphogenesis that accumulate in darkness. In order to test whether light/phy-regulated gene expression occurs through these PIFs, we have performed whole-genome expression analysis in the pif1pif3pif4pif5 quadruple mutant (pifq).
Definition of early transcriptional circuitry involved in light-induced reversal of PIF-imposed repression of photomorphogenesis in young Arabidopsis seedlings.
No sample metadata fields
View SamplesULT1 and CLF function antagonistically as epigenetic regulators of gene expression in Arabidopsis. We sought to identity their global downstream target genes at two stages of plant development and determine their common targets.
The Trithorax Group Factor ULTRAPETALA1 Regulates Developmental as Well as Biotic and Abiotic Stress Response Genes in Arabidopsis.
No sample metadata fields
View SamplesGlobal gene expression data from 7-day old light-grown liquid cultured seedlings treated with or without auxin (5M IAA) for 2 h.
AUXIN RESPONSE FACTOR 2 (ARF2): a pleiotropic developmental regulator.
No sample metadata fields
View SamplesGlobal gene expression data from 7-day old light-grown liquid cultured seedlings treated with or without auxin (5M IAA) for 2 h. Columbia (WT), IAA17 loss of function mutant allele (iaa17-2), IAA17 gain of function mutant allele (axr3-1) and iaa5 iaa6 iaa19 triple loss of function mutant allele (i5i6i19) were used for this study. Each experimental condition has three true replicates for a total of 24 hybridizations. Data
Functional genomic analysis of the AUXIN/INDOLE-3-ACETIC ACID gene family members in Arabidopsis thaliana.
No sample metadata fields
View SamplesRNA samples were extracted from liquid cultured seedlings treated with or without auxin (5M IAA) for 2 h.
Functional genomic analysis of the AUXIN RESPONSE FACTOR gene family members in Arabidopsis thaliana: unique and overlapping functions of ARF7 and ARF19.
No sample metadata fields
View SamplesGlobal gene expression data from 7-day old light-grown liquid cultured seedlings treated with or without auxin (5M IAA) for 2 h. Columbia (WT) and Auxin response factor 2 (ARF2) T-DNA insertion mutant (arf2-6 ) were used for this study. Each experimental condition has three true replicates for a total of 12 hybridizations.
AUXIN RESPONSE FACTOR 2 (ARF2): a pleiotropic developmental regulator.
No sample metadata fields
View SamplesTHO2 and HPR1 proteins were co-depleted from Drosophila S2 cells and their role in mRNA export analysed by comparing total RNA and cytoplasmic RNA
The superhelical TPR-repeat domain of O-linked GlcNAc transferase exhibits structural similarities to importin alpha.
Cell line
View SamplesHuman toxicogenomic studies to date have been of limited size, have mainly addressed exposures at the upper end of typical ranges of human exposure, and have often lacked precise, individual estimates of exposure. Previously, we identified genes associated with exposure to high (>10 ppm) levels of the leukemogen, benzene, through transcriptomic analyses of blood cells from small numbers of occupationally exposed workers. Here, we have expanded the study to 125 workers exposed to a wide range of benzene levels, including <1 ppm. Study design, and analysis with a mixed effects model, removed sources of biological and experimental variability and revealed highly significant widespread perturbation of gene expression at all exposure levels. Benzene is an established cause of acute myeloid leukemia (AML), and may cause one or more lymphoid malignancies in humans. Interestingly, acute myeloid leukemia was among the most significant pathways impacted by benzene exposure in the present study. Further, at most exposure levels, immune response pathways including T cell receptor signaling, B cell receptor signaling, and Toll like receptor signaling were impacted, providing support for the biological plausibility of an association between lymphoma and benzene exposure. We also identified a 16-gene expression signature modified by all levels of benzene exposure, comprising genes with roles in immune response, inflammatory response, cell adhesion, cell-matrix adhesion, and blood coagulation. Overall, these findings support, and expand upon, our current understanding of the mechanisms by which benzene may induce hematotoxicity, leukemia and lymphoma. Furthermore, this study shows that with good study design and analysis, transcriptome profiling of the blood of chemically-exposed humans can identify relevant biomarkers across a range of exposures and inform about potential associations with disease risks.
Global gene expression profiling of a population exposed to a range of benzene levels.
Sex, Age, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Dynamic regulatory network controlling TH17 cell differentiation.
Specimen part, Treatment
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