How does Wingless promote wing disc cell survival?

Our lab has recently shown that Drosophila Wingless (Wg), a key patterning morphogen, is required for cell survival during wing development. The mechanism by which Wg carries out this function is unknown.  Cell death in Drosophila is regulated by a well-defined pathway.  We are exploring how Wg promotes cell survival through the regulation of the genes in this pathway.  For example, Wg may directly or indirectly silence or attenuate pro-apoptotic genes such as hid, reaper or grim.  Conversely, Wg could promote survival by upregulating levels of anti-apoptotic genes such as thread/diap1.  An alternative possibility is suggested by the recent demonstration that discontinuities in morphogen gradients, such as results when Wg signaling is disrupted, can lead to activation of Jun N-terminal kinase (JNK) signaling and to the death of cells, perhaps as a mechanism for correcting mistakes in wing patterning.  Thus Wg activity may prevent activation of the stress-induced JNK pathway.
To determine how Wg specifically controls cell survival, we are modulating Wg activity in small populations of cells in the wing disc.  We find that loss of Wg activity results in increased cell death, increased proliferation and a profound reduction of wing disc size during the third instar.  We are using a combination of genetics and molecular biology to understand these observations and to define how Wg activity regulates cell survival.