Nicotinic acid limitation regulates silencing of Candida adhesins during UTI

Renee Domergue, Irene Castaño, Alejandro De Las Peñas, Margaret Zupancic, Virginia Lockatell, J. Richard Hebel, David Johnson, Brendan P. Cormack

Research output: Contribution to journalArticlepeer-review

Abstract

The adherence of Candida glabrata to host cells is mediated, at least in part, by the EPA genes, a family of adhesins encoded at subtelomeric 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 the limitation of nicotinic acid (NA), a precursor of nicotinamide adenine dinucleotide (NAD+). C. glabrata is an 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 a loss of metabolic capacity and exploitation of the resulting auxotrophy to signal a particular host environment.

Original languageEnglish (US)
Pages (from-to)866-870
Number of pages5
JournalScience
Volume308
Issue number5723
DOIs
StatePublished - May 6 2005

ASJC Scopus subject areas

  • General

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