Nicotinic Acid Limitation Regulates Silencing of Candida Adhesins During UTI.

NIACIN; CANDIDA; GENETIC transcription; URINARY tract infections; NUCLEOTIDES; METABOLISM

The adherence of Candida glabrata to host cells is mediated, atleast in part, by the EPA genes, a family of adhesins encoded atsubtelomeric loci, where they are subject to transcriptional silencing.We show that normally silent EPA genes are expressed during murineurinary tract infection (UTI) and that the inducing signal is thelimitation of nicotinic acid (NA), a precursor of nicotinamide adeninedinucleotide (NAD[sup +]). C. glabrata is an NA auxotroph, andNA-induced EPA expression is likely the result of a reduction in NAD[sup+] availability for the NAD[sup +] -dependent histone deacetylase Sir2p.The adaptation of C. glabrata to the host, therefore, involves a loss ofmetabolic capacity and exploitation of the resulting auxotrophy tosignal a particular host environment. [ABSTRACT FROM AUTHOR]

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