In humans, yeast and other eukaryotes, a group of proteins called the Target of Rapamycin Complex I (TORC1) promote cell growth and increase metabolic activity when nutrients are plentiful. Previous studies have shown how molecules that contain the nutrient nitrogen – which is needed to make proteins – activate TORC1. However, it is not clear how other nutrients regulate this complex. In tackling this problem, James Hughes Hallett, Xiangxia Luo, and Andrew Capaldi in the MCB department found that glucose starvation triggers disassembly of TORC1 and movement of the key TORC1 component Kog1/Raptor into a prion-like aggregate to lock cells in a quiescent (sleep-like) state. The Kog1 aggregates then disassemble in glucose-rich conditions so that cells can grow again. Read more about their work in the journal eLife.