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.
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.
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.
The mesenchyme surrounding the developing brain plays a significant role in controlling the fundamental growth and patterning of the cerebellum, and misregulation of this signalling can lead to important neurodevelopmental disorders.
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.