High impact information on HPT1

• The behavior of adenine auxotrophs bearing additional mutations in purine salvage pathway genes (ade apt1, ade aah1 apt1, ade hpt1) supports a model in which secretion of degradation products, uptake, and reutilization of these products is a signal between cells synchronizing the sporulation process [1].
• Second, overexpression of HPT1 allows suppression of the deregulated phenotype of the guk1 mutants [2].
• Ade4-su, a prototrophic allele of ade4 with reduced activity of PRPPAT, is epistatic to hpt1, suppressing purine excretion and resistance to azaadenine but not resistance to azaguanine [3].
• Hpt1 complements and is not closely linked to the purine excreting mutants pur1 to pur5 [3].
• Xanthine allows both genotypes to grow in the presence of MPA whereas guanine only allows growth of hpt1+ [3].

Associations of HPT1 with chemical compounds

• First, guk1 and hpt1 mutants share several phenotypes, such as adenine derepression, purine excretion, and 8-azaguanine resistance [2].
• Finally, incorporation of hypoxanthine into nucleotides is similarly diminished in hpt1 and guk1 mutants in vivo [2].

Other interactions of HPT1

• Mutants deficient in adenine aminohydrolase (EC 3,5,4,2) activity, aah1, and hypoxanthine:guanine phosphoribosyltransferase (EC 2,4,2,8) activity, hpt1, were used to synthesize the genotypes apt1 hpt1 aah+ and apt1 hpt+ aah1 [4].

References