Fig. 3.

Genetic regulation of G body formation. Hypoxia triggers activation of signaling pathways that are involved in energy homeostasis and required for G body formation (shown on the left). Inhibition of the TORC1 complex by rapamycin treatment prohibits G body formation. In addition to TORC1, Snf1, the yeast ortholog of the AMP-activated protein kinase (AMPK), and Ira2, a negative regulator of the pro-growth pathway (RAS to PKA), is required for G body formation. Hypoxia also triggers the production of superoxide radicals through mitochondrial dysfunction, and the expression of Sod1, the cytoplasmic enzyme that degrades superoxide radicals, is involved in G body formation. Many of the glycolysis enzymes strongly localize to G bodies, including the sequential set of enzymes, PFK and aldolase (see diagram on the right). However, TPI and GAPDH do not strongly localize to G bodies, suggesting the reactions they catalyze occur in the cytoplasm. Downstream of GAPDH, enolase and PYK, catalyzing the final two steps of glycolysis, localize to G bodies, suggesting that both the upstream and far downstream reactions occur in G bodies.