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Vol. 11, Issue 3, 833-848, March 2000
Department of Molecular and Cell Biology, University of California
at Berkeley, Berkeley, California 94720
Glucose performs key functions as a signaling molecule in the yeast
Saccharomyces cerevisiae. Glucose depletion is known to regulate gene expression via pathways that lead to derepression of
genes at the transcriptional level. In this study, we have investigated
the effect of glucose depletion on protein synthesis. We discovered
that glucose withdrawal from the growth medium led to a rapid
inhibition of protein synthesis and that this effect was readily
reversed upon readdition of glucose. Neither the inhibition nor the
reactivation of translation required new transcription. This inhibition
also did not require activation of the amino acid starvation pathway or
inactivation of the TOR kinase pathway. However, mutants in the glucose
repression (reg1, glc7,
hxk2, and ssn6), hexose transporter
induction (snf3 rgt2), and cAMP-dependent protein
kinase (tpk1w and
tpk2w) pathways were resistant to the
inhibitory effects of glucose withdrawal on translation. These findings
highlight the intimate connection between the nutrient status of the
cell and its translational capacity. They also help to define a new
area of posttranscriptional regulation in yeast.
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