Hsf1 and Hsp90 orchestrate temperature-dependent global transcriptional remodelling and chromatin architecture in Candida albicans

Michelle D. Leach, Rhys A. Farrer, Kaeling Tan, Zhengqiang Miao, Louise A. Walker, Christina A. Cuomo, Robert T. Wheeler, Alistair J. P. Brown, Koon Ho Wong and Leah E. Cowen ()
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Michelle D. Leach: Aberdeen Fungal Group, University of Aberdeen, Institute of Medical Sciences
Rhys A. Farrer: Genome Sequencing and Analysis Program, Broad Institute of MIT and Harvard
Kaeling Tan: Faculty of Health Sciences, University of Macau
Zhengqiang Miao: Faculty of Health Sciences, University of Macau
Louise A. Walker: University of Maine
Christina A. Cuomo: Genome Sequencing and Analysis Program, Broad Institute of MIT and Harvard
Robert T. Wheeler: University of Maine
Alistair J. P. Brown: Aberdeen Fungal Group, University of Aberdeen, Institute of Medical Sciences
Koon Ho Wong: Faculty of Health Sciences, University of Macau
Leah E. Cowen: University of Toronto

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Fever is a universal response to infection, and opportunistic pathogens such as Candida albicans have evolved complex circuitry to sense and respond to heat. Here we harness RNA-seq and ChIP-seq to discover that the heat shock transcription factor, Hsf1, binds distinct motifs in nucleosome-depleted promoter regions to regulate heat shock genes and genes involved in virulence in C. albicans. Consequently, heat shock increases C. albicans host cell adhesion, damage and virulence. Hsf1 activation depends upon the molecular chaperone Hsp90 under basal and heat shock conditions, but the effects are opposite and in part controlled at the level of Hsf1 expression and DNA binding. Finally, we demonstrate that Hsp90 regulates global transcription programs by modulating nucleosome levels at promoters of stress-responsive genes. Thus, we describe a mechanism by which C. albicans responds to temperature via Hsf1 and Hsp90 to orchestrate gene expression and chromatin architecture, thereby enabling thermal adaptation and virulence.

Date: 2016
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DOI: 10.1038/ncomms11704

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