From a cross of two strains of Saccharomyces cerevisiae, both of which had the same (wild type or normal) level of resistance to inorganic mercury, segregants having three distinguishable resistance levels, normal, sensitive and semi-sensitive, were obtained. Genetic analyses of the parents and the progeny indicated that the levels of inorganic mercury sensitivity were determined by three distinct loci, HGS1, HGS2 and MSM1. The recessive allele of the HGS1 locus, hgs1-1, and the codominant allele of the HGS2 locus, HGS2-1, were necessary for the sensitive phenotypes, and alleles in the MSM1 locus, MSM1-1 and msm1-2, were responsible for the different sensitivity levels. In short, the strains of genotypes hgs1-1 HGS2-1 msm1-2 and hgs1-1 HGS2-1 MSM1-1 were sensitive and semi-sensitive, respectively, while the strains of all other genotypes were normal. Although the hgs1-1 allele was identified as the aro7-1 mutation which confers deficiency of tyrosine and phenylalanine, mutations such as aro1B (deficiency of tyrosine, phenylalanine and tryptophan) and tyr1 (deficiency of tyrosine) had similar effects as aro7-1 on inorganic mercury sensitivity. From these results we conclude that the HGS2-1 allele causes inorganic mercury sensitivity when the cells are defective in the tyrosine biosynthesis. In fact, addition of tyrosine to the growth medium containing inorganic mercury resulted in increase of colony forming ability of the sensitive strains.

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Journal Article

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Ono B, Sakamoto E

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