Michael Hall Traces TOR's Control of Cell Growth From Yeast Mutants to Human Disease
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Michael Hall, who discovered TOR in 1991 through yeast mutants resistant to rapamycin, explains how this highly conserved protein kinase governs cell growth by size and mass rather than by G1 cell-cycle progression. Rapamycin acts as a complex with FKBP12, binding specific sites on TOR to exert its toxicity. Hall describes two conserved complexes, TORC1 and TORC2, found from yeast to humans. Dysregulation of TOR signaling is linked to cancer, cardiac hypertrophy, obesity and type 2 diabetes, and metformin appears to act partly through TOR inhibition. The account connects the original yeast genetics to present-day therapeutic interest in TOR-targeting drugs.
Written by a model from the reports · updated 2 hours ago
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Michael Hall explains that TOR, a highly conserved protein kinase first identified in 1991 through yeast mutants resistant to rapamycin, controls cell growth by size and mass rather than cell-cycle G1 progression. Rapamycin exerts toxicity as a complex with FKBP12 binding specific sites on TOR. TORC1 and TORC2 are conserved from yeast to humans, and TOR dysregulation links to cancer, cardiac hypertrophy, obesity and type 2 diabetes, with metformin partly acting through TOR inhibition.
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