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E-GEOD-41567 - Expression data from TSA-treated Plasmodium

Released on 13 October 2012, last updated on 22 October 2012
Plasmodium falciparum
Samples (3)
Array (1)
Protocols (8)
Variation of surface adhesins is a critical mediator of virulence and immune evasion in many medically important microbes. Phenotypic switching has been linked to transcriptional changes and the function of chromatin proteins, but the determinants of the rate of phenotypic switching remain poorly defined. We analyzed epigenetic switching of the Plasmodium falciparum erythrocyte invasion ligand PfRh4. By introducing a prokaryotic Dam methylase, we demonstrate that parasites selected for in vivo PfRh4 activation show a reversible increase in promoter accessibility while exhibiting perinuclear repositioning of the locus from a silent to a conserved activation domain. Forced activation of a proximal gene results in a similar level of repositioning of the PfRh4 locus into this domain and a concomitant increase in PfRh4 activation in a sub-population of parasites, with promoter accessibility occurring only at actively transcribed loci. Thus, we reveal two distinct epigenetic mechanisms regulating the expression of a malaria virulence gene. To examine the correlation between changes in gene expression induced by treatment with a high dose of trichostatin A (TSA) and the associated changes in chromatin accessibility. Plasmodium falciparum was treated (or not, control) with 100nm or 500nm TSA, and then the expression profiles were analyzed.
Experiment type
transcription profiling by array 
Elizabeth Ann Winzeler <>, Elizabeth A Winzeler, Micah J Manary
Investigation descriptionE-GEOD-41567.idf.txt
Sample and data relationshipE-GEOD-41567.sdrf.txt
Raw data (1)
Processed data (1)
Array designA-GEOD-16175.adf.txt