Abstract
SummaryJun N-terminal kinase (JNK) often mediates apoptosis in response to cellular stress. However, during normal development, JNK signaling controls a variety of live cell behaviors, such as during dorsal closure in Drosophila embryos. During this process, the latent proapoptotic activity of JNK becomes apparent following Dpp signaling suppression, which leads to JNK-dependent transcriptional activation of the proapoptotic gene reaper. Dpp signaling also protects cells from JNK-dependent apoptosis caused by epithelial disruption. We find that repression of reaper transcription by Dpp is mediated by Schnurri. Moreover, reporter gene analysis shows that a transcriptional regulatory module comprising AP-1 and Schnurri binding sites located upstream of reaper integrate the activities of JNK and Dpp. This arrangement allows JNK to control a migratory behavior without triggering apoptosis. Dpp plays a dual role during dorsal closure. It cooperates with JNK in stimulating cell migration and also prevents JNK from inducing apoptosis.
Highlights
Signaling by c-Jun N-terminal kinase (JNK) mediates one of the major stress response pathways (Chen, 2012; Stronach and Perrimon, 1999)
Little reaper transcription was detectable in crumbs embryos that lack jra or kayak, which encode the two components of AP-1, Jun, and Fos (Figures 1K–1N; see Figures S1F–S1I for reaper expression in the single mutants), and this was associated with a near-absence of apoptosis, as reported by activated caspase-3 immunoreactivity (Figures S1D and S1E)
Neither reaper expression nor apoptosis were significantly activated in the dorsal epidermis, even at the dorsal edge, where JNK signaling is active both in wild-type and crumbs mutants
Summary
During normal development, JNK signaling controls a variety of live cell behaviors, such as during dorsal closure in Drosophila embryos. During this process, the latent proapoptotic activity of JNK becomes apparent following Dpp signaling suppression, which leads to JNK-dependent transcriptional activation of the proapoptotic gene reaper. Dpp signaling protects cells from JNK-dependent apoptosis caused by epithelial disruption. We find that repression of reaper transcription by Dpp is mediated by Schnurri. Dpp plays a dual role during dorsal closure. It cooperates with JNK in stimulating cell migration and prevents JNK from inducing apoptosis
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