Fig. 7

Model of proposed crosstalk between 20E and insulin signaling during metamorphosis in regulating glycometabolism and tissue remodeling. Insulin promotes PGK1 phosphorylation at Y194 to increase glycolysis and cell proliferation (1). 20E represses the expression of PGK1 and dephosphorylates PGK1 via PTEN to suppress glycolysis and cell proliferation (2). 20E induces PGK1 acetylation via ARD1 at K386 to trigger PCD, and insulin stimulates PGK1 deacetylation via HDAC3 (3). High concentrations of 20E antagonize the insulin pathway by switching the phosphorylation of PGK1 to acetylation, thus suppressing glycolysis and inducing autophagy during metamorphosis