Figure 1.

Loss of scrib or dlg function causes defects in specification and differentiation of the PFCs. Wild-type (A, D and G) and mutant egg chambers containing scrib² (B, E and H) or dlg^m52 (C, F and I) clones at the posterior marked by the absence of nuclear GFP (green in B, C, E, F and H) or β-gal (green in I), stained for nuclei (DAPI, blue) and β-gal(red in A-F) or Stau (red in G-I). (A-C) Expression of the PFC marker 998/12 can be observed in stage 10 wild type egg chambers (A, A'), whereas loss of 998/12 expression is evident in the scrib² (B-B") and dlg^m52 (C-C") clone cells. Note that 998/12 is still present in the remaining wild-type posterior cells (B, C), indicating that scrib and dlg act cell-autonomously in specifying the PFCs. (D-F) In the wild type, Kinesin-lacZ is localized at the posterior of the oocyte at stage 9 chambers (D). But the fusion protein is mislocalized to the center when the FCs at the posterior are homozygous for scrib² (E) and dlg^m52 (F). (G-I) In stage 10 wild type egg chambers, Stau accumulates at the posterior of the oocyte (G). Stau is mislocalized to the center as a dot when scrib (H) or dlg (I) is inactivated in FCs at the posterior.