Figure 7.

Model showing developmental timing of Mmp–induced fat body cell dissociation is coordinately and precisely controlled by JH and 20E in Drosophila. During larval–prepupal transition, the anti-metamorphic factor Kr-h1 transduces JH signaling to directly inhibit Mmp expression and to activate timp expression and thus suppresses Mmp–induced fat body cell dissociation. When JH titer declines, the prepupal peak of 20E suppresses Mmp–induced fat body cell dissociation through the 20E primary-response genes, E75 and Blimp-1, which inhibit βftz-F1 expression indirectly or directly. Until 20E titer declines, βftz-F1 expression is induced by the 20E early–late response gene DHR3; then βftz-F1 directly activates Mmp expression and inhibits timp expression and causes Mmp–induced fat body cell dissociation occurring from 6 h APF to 12 h APF. The JH and 20E titers are depicted according to Dubrovsky 2005 (30).