Laboratory study reveals rapid, reversible inhibition of protein synthesis upon glucose withdrawal in yeast, indicating a transcription-independent nutrient-sensing mechanism.
Key Points
To investigate the direct effects of acute glucose depletion and replenishment on protein synthesis and translational control in Saccharomyces cerevisiae.
Monitored rates of protein synthesis in Saccharomyces cerevisiae following rapid glucose withdrawal from the growth medium and subsequent readdition.
Tested requirements for new transcription and evaluated whether the response depends on TOR kinase inactivation or amino acid starvation pathways.
Analyzed translational responses across yeast strains with mutations in glucose repression (reg1, glc7, hxk2, ssn6), hexose transporter induction (snf3 rgt2), and cAMP-dependent protein kinase signaling (tpk1(w), tpk2(w)).
Glucose withdrawal triggered an immediate shutdown of translation that was quickly reversed upon sugar readdition, with neither process requiring new transcription.
Translational inhibition occurred independently of TOR kinase signaling inactivation and amino acid starvation pathway activation.
Mutations in glucose repression, hexose transport induction, and cAMP-dependent protein kinase pathways rendered yeast cells resistant to translation arrest during glucose starvation.