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Nat Commun DOI:10.1038/ncomms11704

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

Publication TypeJournal Article
Year of Publication2016
AuthorsLeach, MD, Farrer, RA, Tan, K, Miao, Z, Walker, LA, Cuomo, CA, Wheeler, RT, Brown, AJP, Wong, KHo, Cowen, LE
JournalNat Commun
Volume7
Pages11704
Date Published2016 May 26
ISSN2041-1723
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.

URLhttp://dx.doi.org/10.1038/ncomms11704
DOI10.1038/ncomms11704
Pubmed

http://www.ncbi.nlm.nih.gov/pubmed/27226156?dopt=Abstract

Alternate JournalNat Commun
PubMed ID27226156
PubMed Central IDPMC4894976
Grant List249793 / / European Research Council / International
BB/F00513X/1 / / Biotechnology and Biological Sciences Research Council / United Kingdom