Nicotinic Acid Limitation Regulates Silencing of Candida Adhesins During UTI
Domergue R, Castano I, De Las Penas A, Zupancic M, Lockatell V, Hebel RJ, Johnson D, Cormack BP
Science (2005)
Category: chromatin structure, dimorphism, epigenetics, flocculation, gene silencing, morphogenesis, sirtuins, yeast pathogens ¤ Added: May 09, 2005 ¤ Rating: ◊◊
Adherence of Candida glabrata to host cells is mediated, at least in part, by the EPA genes, a family of adhesins encoded at sub-telomeric loci where they are subject to transcriptional silencing. We show that normally silent EPA genes are expressed during murine urinary tract infection (UTI) and that the inducing signal is limitation for nicotinic acid (NA), a precursor of NAD+. C. glabrata is a NA auxotroph, and NA-induced EPA expression is likely the result of a reduction in NAD + availability for the NAD+-dependent histone deacetylase Sir2p. The adaptation of C. glabrata to the host, therefore, involves loss of metabolic capacity and exploitation of the resulting auxotrophy to signal a particular host environment.
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