Expression data from Arabidopsis GR-REVOLUTA and KANADI1-GR transgenic seedlings
Ontology highlight
ABSTRACT:
ORGANISM(S): Arabidopsis thaliana
PROVIDER: GSE30702 | GEO | 2013/12/31
SECONDARY ACCESSION(S): PRJNA144361
REPOSITORIES: GEO
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Project description:The REVOLUTA and KANADI1 transcription factors act in opposite directions to control polarity in Arabidopsis. By analyzing mRNA profiles following activation of REVOLUTA or KANADI1 proteins we identified genes regulated by both transcription factors, focusing on those regulated in opposite directions. To coordinate transcriptional responses for microarray analysis, we constructed transgenic seedlings with the REV or KAN1 transcription factor fused to a glucocorticoid receptor (GR) domain. The GR domain tethers the transcription factor in the cytoplasm, and treatment with dexamethasone (DEX) allows movement into the nucleus. Transgenic seedlings and wild-type controls were grown simultaneously in liquid culture, treated with dexamethasone for 0min, 30min, 60min, or 120min, and total RNA was extracted and hybridized to Affymetrix arrays. Treatment: Dexamethasone Biological replicates
2013-12-31 | E-GEOD-30702 | biostudies-arrayexpress
Project description:Unlike the situation in animals, the final morphology of the plant body is highly modulated by the environment. During Arabidopsis development, intrinsic factors provide the framework for basic patterning processes. CLASS III HOMEODOMAIN LEUCINE ZIPPER (HD‐ZIPIII) transcription factors are involved in embryo, shoot and root patterning and during vegetative growth regulate several polarity set‐up processes such as in leaves and the vascular system. Here we show that besides being involved in basic patterning, HD‐ZIPIII transcription factors also have a critical role in controlling elongation growth that is induced when plants experience shade. By using a ChIP‐Seq approach, we have identified several direct target genes of the HD‐ZIPIII transcription factor REVOLUTA (REV). We show that REV acts upstream of auxin biosynthesis and directly regulates several HAT transcription factors that control shade avoidance responses in Arabidopsis. Plants in which HD‐ZIPIII genes are mutated show altered responses to shade revealing that the basic patterning machinery also regulates adaptive development. Thus, HD-ZIPIII transcription factors contribute to shade signaling and act upstream of both auxin and HAT activation. A. thaliana REVOLUTA ChIP-seq w control
2012-06-01 | E-GEOD-26722 | biostudies-arrayexpress
Project description:Unlike the situation in animals, the final morphology of the plant body is highly modulated by the environment. During Arabidopsis development, intrinsic factors provide the framework for basic patterning processes. CLASS III HOMEODOMAIN LEUCINE ZIPPER (HD‐ZIPIII) transcription factors are involved in embryo, shoot and root patterning and during vegetative growth regulate several polarity set‐up processes such as in leaves and the vascular system. Here we show that besides being involved in basic patterning, HD‐ZIPIII transcription factors also have a critical role in controlling elongation growth that is induced when plants experience shade. By using a ChIP‐Seq approach, we have identified several direct target genes of the HD‐ZIPIII transcription factor REVOLUTA (REV). We show that REV acts upstream of auxin biosynthesis and directly regulates several HAT transcription factors that control shade avoidance responses in Arabidopsis. Plants in which HD‐ZIPIII genes are mutated show altered responses to shade revealing that the basic patterning machinery also regulates adaptive development. Thus, HD-ZIPIII transcription factors contribute to shade signaling and act upstream of both auxin and HAT activation.
2012-06-01 | GSE26722 | GEO
Project description:We extracted RNA of sorted splenic CD11b+Gr-1+ cells and performed microarray analyses. Total RNA was isolated using the manufacturer’s recommended protocol for RNeasy (Qiagen, Valencia, CA). Isolated RNA was quantified, and quality was assessed using an Agilent A 2100 BioAnalyzer with the RNA NanoChip (Agilent, Andover, MA). We used 2μg of total RNA to make single-stranded antisense cDNA with the NuGEN Technologies (San Carlo, CA) Ovation Biotin System in accordance with the manufacturer’s directions. Labeled targets were hybridized to Affymetrix (Santa Clara, CA) MOE430 2.0 GeneChip microarrays for 16h at 45°C. The arrays were washed and scanned according to Affymetrix standard protocols. We used microarrays to detail the global gene expression of CD11b+Gr-1+ cells from the control mice and the clarithromycin-treated mice, and identified distinct classes of up-regulated genes during this process.
2016-05-09 | GSE81241 | GEO
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2014-10-23 | GSE53470 | GEO
Project description:QKI regulated splicing required for cell polarity
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Project description:A group of postnatal neurodevelopmental disorders collectively referred to as MeCP2 disorders are caused by aberrations in the gene encoding methyl-CpG-binding protein 2 (MECP2). Loss of MeCP2 function causes Rett syndrome (RTT), whereas increased MeCP2 dosage causes MECP2 duplication or triplication syndromes. MeCP2 acts as a transcriptional repressor, however, the gene expression changes observed in the hypothalamus and cerebellum of MeCP2 disorder mouse models suggest that MeCP2 can also upregulate gene expression. In this study, we compared gene expression changes in the amygdalae of mice lacking MeCP2 (Mecp2-null) and mice overexpressing MeCP2 (MECP2-TG). We chose the amygdala because it is a neuroanatomical region implicated in the control of anxiety and social behavior, two prominent phenotypes in MECP2-TG mice, and hypothesized that transcriptional profiling of this particular brain region may reveal expression changes relevant to heightened anxiety-like behavior and abnormal social behavior. A total of 1,060 genes were altered in opposite directions in both MeCP2 mouse models compared with wild-type littermates, with ~60% up-regulated and ~40% down-regulated. Interestingly, we found a significant enrichment of anxiety- and/or social behavior-related genes among the differentially expressed genes. To determine whether these genes contribute to the anxiety and social behavior phenotypes in MECP2-TG mice, we performed genetic and pharmacologic studies and found that a reduction in Crh suppresses anxiety-like behavior, and a reduction in Oprm1 improves social approach behavior. These studies suggest that MeCP2 impacts molecular pathways involved in anxiety and social behavior, and provide insight into potential therapies for MeCP2 disorders. This study is published in Nature Genetics http://dx.doi.org/10.1038/ng.1066.
2012-01-08 | GSE33457 | GEO
Project description:Purpose: The goals of this study are screening the putative target genes regulated by OsNF-YA5 using DEX(dexamethason) inducible system. Methods: 10-day-old GOS2::OsNF-YA5-GR plants grown on MS solid media were treated with 50 μM dexamethasone (DEX) solution containing 0.02% (w/v) Silwet L-77. For mock treatments, 0.02% Silwet L-77 was sprayed into rice plants. To minimize the effect by the treatment, plants were pre-treated with 0.02% Silwet L-77 3 hours before DEX treatment). Total RNAs were extracted using the RNeasy plant mini kit (Qiagen, USA) according to the manufacturer’s instruction. cDNA libraries were prepared using the TruSeq RNA Sample Prep kit (v2) (Macrogen, Korea). Single-end sequences were obtained using IRGSP (v 1.0) and raw sequence reads were trimmed to remove adaptor sequence, and those with a quality lower than Q20 were removed using the Trimmomatic 0.32 software (Bolger et al., 2014). To map the reads to reference genome, all reads were assembled with annotated genes from the Rap-DB database [http://rapdb.dna.affrc.go.jp; IRGSP (v 1.0)] using TopHat software (https://ccb.jhu.edu/software/tophat/index.shtml). After mapping reads to a reference genome, differentially expressed genes (DEGs) were selected using a cut-off change of at least 2-fold change (DEX/mock) and Student’s t-test (P < 0.1). The selected DEGs were grouped by hierarchical clustering analysis (Complete Linkage). Results: RNA sequencing analysis revealed that 81 (3 hr DEX treatment) and 88 (9 hr DEX treatment) genes were up-regulated. In comparison, 61 (3 hr DEX treatment) and 45 (9 hr DEX treatment) genes were down-regulated in GOS2:OsNF-YA5-GR transgenic plants by DEX treatment compared to mock treatment. Among 161 up-regulated genes, 71 genes (44%) were also up-regulated in N starvation conditions. GO term analysis of up-regulated genes revealed that 59-76% of genes were involved in the metabolic process, and 10%-12% were transporter (Extended Data Fig. 4c). These results suggested that OsNF-YA5 regulated the genes involved in the metabolic process. Conclusions: OsNF-YA5 positively regulated the genes involved in the nitrogen metabolic process including amino acid and nitrate/peptide transporters.
2024-01-03 | GSE178682 | GEO
Project description:A group of postnatal neurodevelopmental disorders collectively referred to as MeCP2 disorders are caused by aberrations in the gene encoding methyl-CpG-binding protein 2 (MECP2). Loss of MeCP2 function causes Rett syndrome (RTT), whereas increased MeCP2 dosage causes MECP2 duplication or triplication syndromes. MeCP2 acts as a transcriptional repressor, however, the gene expression changes observed in the hypothalamus and cerebellum of MeCP2 disorder mouse models suggest that MeCP2 can also upregulate gene expression. In this study, we compared gene expression changes in the amygdalae of mice lacking MeCP2 (Mecp2-null) and mice overexpressing MeCP2 (MECP2-TG). We chose the amygdala because it is a neuroanatomical region implicated in the control of anxiety and social behavior, two prominent phenotypes in MECP2-TG mice, and hypothesized that transcriptional profiling of this particular brain region may reveal expression changes relevant to heightened anxiety-like behavior and abnormal social behavior. A total of 1,060 genes were altered in opposite directions in both MeCP2 mouse models compared with wild-type littermates, with ~60% up-regulated and ~40% down-regulated. Interestingly, we found a significant enrichment of anxiety- and/or social behavior-related genes among the differentially expressed genes. To determine whether these genes contribute to the anxiety and social behavior phenotypes in MECP2-TG mice, we performed genetic and pharmacologic studies and found that a reduction in Crh suppresses anxiety-like behavior, and a reduction in Oprm1 improves social approach behavior. These studies suggest that MeCP2 impacts molecular pathways involved in anxiety and social behavior, and provide insight into potential therapies for MeCP2 disorders. This study is published in Nature Genetics http://dx.doi.org/10.1038/ng.1066. Total amygdala RNA samples were collected from Mecp2-null male mice (n=4), MECP2-transgenic male mice (n=5), and their wild type male littermates at 6 weeks of age (n=4, n=5 for each group respectively).
2012-01-08 | E-GEOD-33457 | biostudies-arrayexpress