Arabidopsis thaliana
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ABSTRACT:
PROVIDER: PRJNA100573 | ENA |
REPOSITORIES: ENA
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Project description:Calcium responsiveness in Arabidopsis using calmodulin antagonists
| PRJNA96167 | ENA
Project description:Genome-wide binding analysis of Arabidopsis GATA transcription factors GNC and CGA1
| PRJNA382131 | ENA
Project description:Calcium has been shown to be an important signalling molecule in the transduction of abiotic stress signals in Arabidopsis thaliana. Alteration of the calcium signature through the use of inhibitors has been shown to result in changes in the expression of certain downstream abiotic stress-induced genes. However, the communication of this signal through specific calcium-sensitive intermediate molecules has remained poorly elucidated. Various candidate molecules exist and including calcinurin, calcium-dependent protein kinases and calmodulin. Recently, a screen of an Arabidopsis thaliana cDNA expression library with calmodulin resulted in the isolation of the protein designated calmodulin-binding transcriptional activator or AtCAMTA that may function as one of these calcium-sensitive intermediate molecules. The Arabidopsis genome contains six CAMTA genes (AtCAMTA1-6), all of which are expressed in varying tissues throughout development. AtCAMTA1 was shown to function as a transcriptional activator through the expression of a chimeric protein consisting of the bacteria LexA protein fused to various segments of AtCAMTA expressed in yeast. In order to identify putative target genes of AtCAMTA1 in Arabidopsis we plan to analyse the transcriptome of AtCAMTA1 loss-of-function mutants. The gene expression pattern of two previously characterised alleles of AtCAMTA1 will be compared to wild type. Experimenter name = Sarah Scrase-Field; Experimenter phone = 01865 275062; Experimenter fax = 01865 275074; Experimenter department = University of Oxford; Experimenter address = Department of Plants Sciences; Experimenter address = University of Oxford; Experimenter address = South Parks Road; Experimenter address = Oxford; Experimenter zip/postal_code = OX1 3RB; Experimenter country = UK Experiment Overall Design: 4 samples were used in this experiment
2008-06-13 | E-GEOD-5618 | biostudies-arrayexpress
Project description:Effect of CaM overexpression on Arabidopsis transcriptome. Unlike animals, plants are immobile and cannot simply move away from unfavourable environments and thus have developed complex mechanisms to respond to and sense biotic and abiotic signals. These stimuli often lead to tightly controlled changes in cytoplasmic free calcium concentration [Ca2+]cyt termed "calcium signatures" which are thought to be, at least partly, responsible for the specificity of plant responses to the environment. However little is known about how exactly these calcium signatures are decoded into specific end-responses. Calmodulin (CaM) is the most well characterised Ca2+ binding protein and is the primary sensor of changing [Ca2+]. Upon binding Ca2+ CaM undergoes a conformational change allowing binding and activation of a wide variety of target proteins. In plants CaM exists in gene families encoding multiple isoforms. The expression of individual CaM genes can be differentially regulated and isoforms may be differentially localised. Furthermore specific isoforms can bind and activate different target proteins. These features of plant CaM allow the possibility of specificity during calcium signalling in response to specific stimuli. The effect of overexpression of four CaM protein isoforms on the Arabidopsis thaliana transcriptome will be investigated. Ten day old transgenic Arabidopsis seedlings (containing estradiol inducible CaM overexpression constructs) were induced for 9hrs in 5uM estradiol with appropriate water (0.025% DMSO) and empty vector controls.
2008-02-15 | E-NASC-65 | biostudies-arrayexpress
Project description:Calcium signaling is a central regulator of cardiomyocyte growth and function. Calmodulin is a critical mediator of calcium signals. Because the amount of calmodulin within cardiomyocytes is limiting, precise regulation of calmodulin expression may be an important for regulation of calcium signaling. In this study, we show for the first time that calmodulin levels are regulated post-transcriptionally in heart failure. The cardiomyocyte-restricted microRNA miR-1 inhibited translation of calmodulin-encoding mRNAs via highly conserved target sites within their 3’-untranslated regions. In keeping with its effect on calmodulin expression, miR-1 downregulated calcium-calmodulin signaling through the calcineurin to NFAT. miR-1 also negatively regulated expression of Mef2a and Gata4, key transcription factors that mediate calcium-dependent changes in gene expression. Consistent with downregulation of these hypertrophy-associated genes, miR-1 attenuated cardiomyocyte hypertrophy in cultured neonatal rat cardiomyocytes and in the intact adult heart. Our data indicate that miR-1 regulates cardiomyocyte growth responses by negatively regulating the calcium-signaling components calmodulin, Mef2a, and Gata4.
2009-03-05 | GSE13874 | GEO
Project description:ChIP-seq for Polycomb and associated transcription factors in Arabidopsis
| PRJNA329443 | ENA
Project description:Genome-Wide binding sites of two MADS-domain transcription factors SOC1 and SVP in Arabidopsis during the floral transition
| PRJNA149273 | ENA
Project description:The formation of long-term memory requires signaling from the synapse to the nucleus to mediate neuronal activity-dependent gene transcription. Synapse-to-nucleus communication is initiated by influx of calcium ions through synaptic NMDA receptors and/or L-type voltage-gated calcium channels and involves the activation of transcription factors by calcium/calmodulin signaling in the nucleus. Recent studies have drawn attention to a new family of transcriptional regulators, the so-called calmodulin-binding transcription activator (CAMTA) proteins. CAMTAs are expressed at particularly high levels in the mouse and human brain, and we reasoned that, as calmodulin-binding transcription factors, CAMTAs may regulate the formation of long-term memory by coupling synaptic activity and calcium/calmodulin signaling to memory-related transcriptional responses. This hypothesis is supported by genetic studies that reported a correlation between CAMTA gene polymorphisms or mutations and cognitive capability in humans. Here, we show that acute knock-down of CAMTA1, but not CAMTA2, in the hippocampus of adult mice results in impaired performance in two memory tests, contextual fear conditioning and object-place recognition test. Short-term memory and neuronal morphology were not affected by CAMTA knock-down. Gene expression profiling in the hippocampus of control and CAMTA knock-down mice revealed a number of putative CAMTA1 target genes related to synaptic transmission and neuronal excitability. Patch clamp recordings in organotypic hippocampal slice cultures provided further evidence for CAMTA1-dependent changes in electrophysiological properties. In summary, our study provides experimental evidence that confirms previous human genetic studies and establishes CAMTA1 as a regulator of long-term memory formation.
2016-05-20 | GSE62122 | GEO
Project description:Analysis of transcription factor HY5 genomic binding sites in Arabidopsis
| PRJNA98687 | ENA