GLUCOSE-UPTAKE AND CATABOLITE REPRESSION IN DOMINANT HTR1 MUTANTS OF SACCHAROMYCES-CEREVISIAE

Growth and carbon metabolism in triosephosphate isomerase (DELTAtpi1) mutants of Saccharomyces cerevisiae are severely inhibited by glucose. By using this feature, we selected for secondary site revertants on g lucose. We defined five complementation groups, some of which have pre viously been identified as glucose repression mutants. The predominant mutant type, HTR1 (hexose transport regulation), is dominant and caus es various glucose-specific metabolic and regulatory defects in TPI1 w ild-type cells. HTR1 mutants are deficient in high-affinity glucose up take and have reduced low-affinity transport. Transcription of various known glucose transporter genes (HXT1, HXT3, and HXT4) was defective in HTR1 mutants, leading us to suggest that HTR mutations affect a neg ative factor of HXT gene expression. By contrast, transcript levels fo r SNF3, which encodes a component of high-affinity glucose uptake, wer e unaffected. We presume that HTR1 mutations affect a negative factor of HXT gene expression. Multicopy expression of HXT genes or parts of their regulatory sequences suppresses the metabolic defects of HTR1 mu tants but not their derepressed phenotype at high glucose concentratio ns. This suggests that the glucose repression defect is not a direct r esult of the metabolically relevant defect in glucose transport. Alter natively, some unidentified regulatory components of the glucose trans port system may be involved in the generation or transmission of signa ls for glucose repression.