Figure 1.

Linking the insulin-like, AMPK and TOR signaling pathways upstream of GSC quiescence. Upon insulin-like receptor activation, PtdInsP3 kinase (PI3K) phosphorylates PtdInsP₂. This activity is counteracted by PtdInsP3 phosphatase (DAF-18/PTEN). PtdInsP₃ activates, in a PDK-1/PDK1-dependent manner AKT/Akt, which phosphorylates and thereby prevents the nuclear translocation of the DAF-16/FOXO transcription factor. In Drosophila and mammals, Akt and AMPK act antagonistically to regulate TOR signaling through inhibitory and activating phosphorylation of TSC2, respectively. Arrows indicate activation; bars inhibition. Based on [11, 59, 85, 87, 88].