Genetic control of metabolism of the mutagenic base analogue 6-Af-hydroxylaminopurine in yeast saccharomyces cerevisiae

Yeasts were shown to utilize 6-substituted adenine analogues as a purine source via the reutilization pathway leading to the formation of inosine monophosphate (IMP). This occurs because the ade!2 strains with blocked conversion of IMP into adenosine monophosphate (AMP) cannot grow on media containing the above analogues as a sole purine source. Haploid strains with the double mutation hamlade2 or HamladeS were also incapable of growing on a medium with 6-Af-hydroxylaminopurine (HAP) as a sole purine source. However, in this case, this inability was caused by the occurrence of recessive lethal mutations rather than by a defect in purine reutilization. Yeast adenine aminohydrolase (AAH) can deaminate HAP to hypoxanthine. Adenine aminohydrolase (AAH) was uniformly active both in strains with a mutation in the HAM1 gene and in strains wildtype with respect to this trait.