Hypoxanthine: guanine phosphoribosyltransferase mutants in Saccharomyces cerevisiae.

摘要: Yeast mutants lacking activity of the enzyme hypoxanthine: guanine phosphoribosyltransferase (H:GPRT) have been isolated by selecting for resistance to 8-azaguanine in a strain carrying wild type allele, ade4+ gene coding amidophosphoribosyltransferase (PRPPAT), first de novo purine synthesis. The excrete purines and are cross-resistant 8-azaadenine. They recessive represent single complementation group, designated hpt1. Ade4-su, prototrophic allele ade4 with reduced PRPPAT, is epistatic hpt1, suppressing excretion azaadenine but not azaguanine. genotype ade2 hpt1 does respond hypoxanthine. Hpt1 complements closely linked excreting pur1 pur5. pur6, regulatory mutant also unlinked do complement, suggesting protein-protein interaction between H:G-PRT PRPPAT. Mycophenolic acid (MPA), an inhibitor nucleotide synthesis, inhibits growth hpt1+. Xanthine allows both genotypes grow presence MPA whereas only Activity A-PRT, X-PRT present hpt+. lacks has normal A-PRT X-PRT.