In Drosophila melanogaster, nutrition controls body size by acting through the Forkhead Box class O (FoxO)/Ultraspiracle complex to regulate nutrition-sensitive ecdysone biosynthesis, thereby controlling the switch to stop growth.
The basic helix-loop-helix transcription factor, HES3, acts downstream of the PAX3-FOXO1 fusion oncogene to impair muscle differentiation and promote tumorigenesis in rhabdomyosarcoma, a childhood muscle cancer.
Stimulation of endothelial glucose metabolism and vascular growth by genetic depletion of endothelial Foxo1 improves the whole-body response to a high-fat diet, by preserving adipose tissue functions and glucose homeostasis.
Structural and biochemical analysis reveals that two intrinsically disordered domains of the transcription factor FoxM1 co-fold to form an autoinhibited conformation, which is disrupted by a specific activating phosphorylation event.
A signaling pathway involving PGAM5, ASK1 and JNK induces persistent FoxO activation, chaperone expression and lifespan extension following developmental mitochondrial stress, which can be blocked by mTOR signaling through GCN-2.