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SHR3

Per O. Ljungdahl, Gerald R. Fink

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Abstract

Abstract Spontaneous yeast mutants resistant to 30 mM histidine were isolated1· Genetic analysis indicates that super high histidine resistant (shr} mutants resulted from recessive mutations in single genes defining nine complementation groups. Mutations in the SHR3 gene confer resistance to high concentrations of histidine by pleiotropically inhibiting the functional expression of the general amino acid permease (GAP1} and at least 10 specific high affinity amino acid permeases.

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What this paper is about

Abstract Spontaneous yeast mutants resistant to 30 mM histidine were isolated1· Genetic analysis indicates that super high histidine resistant (shr} mutants resulted from recessive mutations in single genes defining nine complementation groups. Mutations in the SHR3 gene confer resistance to high concentrations of histidine by pleiotropically inhibiting the functional expression of the general amino acid permease (GAP1} and at least 10 specific high affinity amino acid permeases.

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Available abstract

Abstract Spontaneous yeast mutants resistant to 30 mM histidine were isolated1· Genetic analysis indicates that super high histidine resistant (shr} mutants resulted from recessive mutations in single genes defining nine complementation groups. Mutations in the SHR3 gene confer resistance to high concentrations of histidine by pleiotropically inhibiting the functional expression of the general amino acid permease (GAP1} and at least 10 specific high affinity amino acid permeases.

Key concepts: Complementation, Histidine, Permease, Mutant, Gene, Amino acid, Yeast, Biology

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