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. Author manuscript; available in PMC: 2016 Mar 22.
Published in final edited form as: Nature. 2003 May 8;423(6936):181–185. doi: 10.1038/nature01578

Figure 4.

Figure 4

Manipulation of nicotinamide metabolism alters silencing and lifespan. a, To monitor silencing, ADE2 was integrated at the rDNA locus. Increased growth on medium lacking adenine indicates decreased silencing. Serial dilutions of cells spotted on plates containing nicotinic acid or nicotinamide (5 mM). b, PNC1 does not have a critical role in NAD+ biosynthesis, even in the absence of the de novo NAD+ synthesis pathway. BNA6 encodes an enzyme in the NAD+ de novo synthesis pathway (see Fig. 1b). NPT1 encodes a phosphoribosyltransferase that converts nicotinic acid to nicotinic acid mononucleotide in the NAD+ salvage pathway. Spore colonies from heterozygous bna6Δ npt1Δ or bna6Δ pnc1Δ diploids. Genotypes determined by PCR with a colony/ microcolony genomic template. c, Partial rescue of silencing by additional PNC1 in the absence of the NAD+ salvage pathway and complete rescue in the presence of quinolinic acid (5 mM). d, Manipulation of genes involved in nicotinamide metabolism alters rDNA silencing. e, Manipulation of YLR285W affects lifespan. f, Model for the regulation of Sir2 activity and lifespan by PNC1 and nicotinamide (NAM).