Embryonic diapause, which in mammals refers to development pausing at the blastocyst stage, is thought to conserve energy during times of environmental stress. Diapause can also be induced by inhibiting mTOR signalling, but the specific mechanisms linking environmental stress to diapause remain unclear. Here, Qiang Sun and colleagues explore how nutrient depletion induces embryonic diapause in mice. They show that embryos from mice that were starved in early pregnancy do not implant and are arrested at the blastocyst stage. Using immunofluorescence staining, they find that downstream markers of mTORC1 activity are almost undetectable in these embryos. Blastocysts taken from mice on a standard diet survive longer in vitro and exhibit signs of diapause induction when their culture medium is depleted of either protein or carbohydrates. By restoring each depleted component to the culture medium individually, the authors identify Arginine, Leucine, Isoleucine, Lysine, Glucose and Lactate (ALILGL) as the key protein and carbohydrate components, depletion of which leads to diapause. Importantly, they find that the concentration of ALILGL in uterine fluid decreases during mouse embryonic diapause. Depletion of protein and carbohydrates does not trigger diapause in embryos lacking Gator1 or Tsc2, known sensors of amino acid and glucose deprivation, respectively. Overall, this work identifies key nutrients, depletion of which can trigger embryonic diapause via the nutrient sensors Gator1 and Tsc2, which appear to sit upstream of the mTOR pathway.