Fig. 6

Neur-dependent Dl-signalling prevents a neurogenic phenotype of homozygous Dl^attP-DlK2R-HA flies. A–C Analysis of Dl^attP-DlK2R-NEQN2A-HA. A Cuticle preparation of a homozygous Dl^attP-DlK2R-NEQN2A-HA embryo. It shows the severe reduction of cuticle (arrow) that is characteristic for the neurogenic phenotype. B–C’ Clonal analysis of Dl^attP-DlK2R-NEQN2A-HA in wing discs. Clones are labelled by the loss of GFP. Supernumerary SOPs, labelled by Hnt-expression, develop in the homozygous Dl^attP-DlK2R-NEQN2A-HA clones in the notum (arrows) and the anterior wing margin (arrowhead), indicating that Dl^attP-DlK2R-NEQN2A cannot mediate the Neur-dependent selection of the SOP. C, C’ Magnification of the notal region highlighted in A with the arrows. It reveals that the developing SOPs accumulate DlK2R- NEQN2A-HA in their plasma membranes to high levels (arrows). D, D’ A wing disc bearing large homozygous DlattP-DlK2R-HA clones, labelled by loss of GFP and outlined in white. The arrow points to the SOP at the prominent halo of Gbe + Su(H) expression surrounding the emerging SOP at the tr1/APA position in the homozygous clones. The halo reveals the presence of Neur-mediated signalling of the ligands. E–E’’’ A wing disc bearing Neur-expressing MARCM clones which are also homozygous for Dl^attP-DlK2R-HA (genotype: hsFlp tubGal4 UAS GFPnls; + / UAS neur; FRT 82B tubGal80/ FRT82B Dl^attP-DlK2R-HA). The arrow in E, E’ points to a Dl^attP-DlK2R-HA homozygous clone shown at higher magnification in the z-section in E’’. In contrast to Dl^attP-DlK2R-HA clones, the abundance of DlK2R in the plasma membrane (E’) is strongly reduced if Neur is additionally expressed. E’’’ Pixel intensity measurement of the apical region including the clone shown in E’’. The levels of apical Dl are reduced in the GFP-positive MARCM clone (high GFP). Note, that an increase in the abundance of DlK2R-HA is normally observed in the homozygous cells (see Fig. 3A–A’’’)