S. Ozcan et al., GLUCOSE-UPTAKE AND CATABOLITE REPRESSION IN DOMINANT HTR1 MUTANTS OF SACCHAROMYCES-CEREVISIAE, Journal of bacteriology, 175(17), 1993, pp. 5520-5528
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.