Nicotinic acid limitation regulates silecing of Candida adhesins during UTI
Nicotinic acid limitation regulates silecing of Candida adhesins during UTI
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DOI：
10.1126/science.1108640
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发表时间：
2005-05-06
期刊：
影响因子：
56.9
通讯作者：
Cormack, BP
中科院分区：
文献类型：
--
作者：
Domergue, R;Castaño, I;Cormack, BP
光滑念珠菌对宿主细胞的粘附至少部分由EPA基因介导，EPA基因是在亚端粒位点编码的粘附素家族，在那里它们受到转录沉默。我们发现，通常沉默的EPA基因表达在小鼠尿路感染（UTI）和诱导信号是限制烟酸（NA），烟酰胺腺嘌呤二核苷酸（NAD（+））的前体。C. glabrata是NA营养缺陷型，NA诱导的EPA表达可能是NAD（+）依赖性组蛋白脱乙酰酶Sir2p的NAD（+）可用性降低的结果。C.因此，光滑的宿主的代谢缺陷涉及代谢能力的丧失和利用所产生的营养缺陷型来发出特定宿主环境的信号。
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.