JNK and decapentaplegic signaling control adhesiveness and cytoskeleton dynamics during thorax closure in Drosophila

One of the fundamental events in metamorphosis in insects is the replacemen t of larval tissues by imaginal tissues. Shortly after pupariation the imag inal discs evaginate to assume their positions at the surface of the prepup al animal. This is a very precise process that is only beginning to be unde rstood. In Drosophila, during embryonic dorsal closure, the epithelial cell s push the amnioserosa cells, which contract and eventually invaginate in t he body cavity, In contrast, we find that during pupariation the imaginal c ells crawl over the passive larval tissue following a very accurate tempora l and spatial pattern. Spreading is driven by filopodia and actin bridges t hat, protruding from the leading edge, mediate the stretching of the imagin al epithelia, Although interfering with JNK (Jun N-terminal kinase) and dpp (decapentaplegic) produces similar phenotypic effects suppressing closure, their effects at the cellular level are different. The loss of JNK activit y alters the adhesion properties of larval cells and leads to the detachmen t of the imaginal and larval tissues. The absence of dpp signaling affects the actin cytoskeleton, blocks the emission of filopodia, and promotes the collapse of the leading edge of the imaginal tissues. Interestingly, these effects are very similar to those observed after interfering with JNK and d pp signaling during embryonic dorsal closure.