Abl potentially regulates CycE expression via the Hippo pathway.

(A-C) In wild type neuroblasts stained with Dpn (blue) at stage 11 (A) a stable expression of Salvador (Sav, red) can be observed mirroring the active Hpo kinase. Mutation in Abl⁴ (B) or double mutation in lab¹ and Dfd¹² (C) show reduced Sav protein distribution, which argues for a less stable protein and an inactive Hpo kinase. Lower panel shows Sav channel in monochrome. (D) Yorkie (magenta) is localized to the cytoplasm of NB6-4max prior to its first division at stage 10. Cytoplasmically localized Yki is the inactive form of Yki. (E) Ectopic expression of a constitutive active form of Yki^CA using the scabrous-Gal4 (scaGal4) line transforms NB6-4max in 29% of all maxillary hemisegments. (F) Triple mutation for yki^B5 and Abl⁴,Dfd¹⁶, shows a decrease in the transformation rate from 100% in the double mutants for Abl⁴,Dfd¹⁶ to 69% in the triple mutants. Thus, the loss of yki rescues the double mutant phenotype in 31% of all hemisegments. (G) Schematic model of the cell-autonomous and non-cell-autonomous regulation of maxillary identity specification of NB6-4. Expression pattern of Antp-C genes are shown color-coded in the CNS. In the posterior part of the maxillary segment Dfd and Scr are co-expressed. Lab, Dfd and Antp positively regulate the expression of Ama (brown areas and arrows), whereas Scr represses Ama expression. Ama binds to Nrt and via Dab activates Abl that leads to the repression of CycE expression presumably through the Hippo/Salvador/Warts pathway. Whether Abl influences the Hpo kinase or Yki itself needs to be further clarified. Scale bar is 10 μm.